ristojkoivula

Miksi "peilisolu" ("mirror neuron") on epätosi ja tuhoisa valekäsite

  • Miksi "peilisolu" ("mirror neuron") on epätosi ja tuhoisa valekäsite

https://www.worldsciencefestival.com/2014/08/smart-reads-gregory-hickoks-myth-mirror-neurons/

https://www.amazon.com/Myth-Mirror-Neurons-Neuroscience-Communication/dp/0393089614

 

The Myth of Mirror Neurons:

The Real Neuroscience of Communication and Cognition 1st Edition

by Gregory Hickok (Author)

https://www.youtube.com/watch?v=MtEjYs_hLYw

https://www.worldsciencefestival.com/2014/08/smart-reads-gregory-hickoks-myth-mirror-neurons/

https://hameemmias.vuodatus.net/lue/2015/10/europuoskaritiedetta-suomen-tieteen-huippuyksikossa-ka-2004

 

Mirror neurons are a myth and professor Hickok brings a lot of relevant questions in tis book that most would find boring as hell unless you have a clever insight and interest in the working of the brain. of course I stull like my theory that the real creature of all humanity and species are of course the brain and flesh and other structures just shell castings. Some brains are more highly developed and more specialized physical properties to accomplish physics on earth and the real mystery of the cosmos can somehow be traced to the brain.

 Greg Hickok)

The fact that many scientists were quick to jump on this theory and put blame for everything to altu-sim to altruism dismayed professor Hickok to such an incredible degree that he hard wired a book of this nature to attack the mirror neuron hypothesis. one can just find old episodes of Gilligan's Island and Hogan's Heroes to see how easily chimps can be manipulated to act and move about imitating their taller cousins with more complex ahhh brain development. Of course relying your theories from gay caged monkies and gorillas also is bullshit as the complexities of human cognition and brain functions shouldn't be relied so heavily on the actions of hungry, smaller primates acting out in a confined area in front of researchers, scientists, and professors hungry for state funding and grants to cast their ideas and spells.

 

http://ristojkoivula.puheenvuoro.uusisuomi.fi/257298-opetushallitus-opettaa-kumottua-jarjetonta-peilineurooniteoriaa-opettajille#comment-3890896

Greg Hickok: The myth of mirror neurons

Relational Implicit

January 2015

Gregory Hickok, Ph.D.is Professor of Cognitive Sciences at UC Irvine,Founder, Director Emeritus, and current Fellow of the UCI Center for Cognitive Neuroscience & Engineering, Founder and Direc-tor of the Center for Language Science, Fellow of the Center for the Neurobiology of Learning & Memory and the Center for Hearing Research, and past Chair of the Research Imaging Center’s Imaging Steering Committee.

Beyond UCI he is the founding President of the Society for the Neurobiology of Language, Editor-in-Chief of Psychonomic Bulletin & Review, and author of The Myth of Mirror Neurons:

 

https://relationalimplicit.com/zug/transcripts/Hickok-2015-01.pdf

The Real Neuroscience of Communication and Cognition.

This is part of the Relational Implicit project, edited by Serge Prengel.

For better or worse, this transcript retains the spontaneous, spoken-language quality of the podcast conversation.

 

Serge Prengel: Hi Greg.

Gregory Hickok: Hi there, Serge.

 

Serge: So you wrote a book about mirror neurons and demystifying their role. Maybe we can start with the beginning. What are mirror neurons?

Gregory: Sure. Mirror neurons are cells in the motor cortex or motor system of Macaque monkeys.

They were discovered in the context of doing some basic research on motor control, trying to figure out how Macaque monkeys and, by generalization, humans may code movement plans in terms of object-based coordinates.That is,when you reach for an object you have to take in information about the object’s shape and location and size into account to guide your reach. You pre-shape your hand when reaching for a cup versus a pen, for example. And so Giacomo Rizzolatti from Parma and his group were studying this process in macaques and they had discovered a class of cells in a motor area known as F5 for frontal area number five that seemed to respond or that did respond both during reaching behaviors and during the observation of object shape.

[RJK:  Rizzolattin havaintoja ei ole pystytty toistamaan sellaisenaan makakeilla - eikä millään muilla-kaan lajeilla. Hänen koepöytäkirjana ovat salaisia sosiobiologistikirkon sisimmiltäkin piireiltä, paljasti niiden silloinen jäsen Michael Arbib yli 10 vuotta sitten.

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/152521?page=1#152521
 

RK  16.06.2005 01:47:09
176429

Rizzolattin "peiliSOLUhavaintoja" ei ole pystytty vahvistamaan.

Harmis löysi viestissä 176090 milenkiintoisen linkin sosiobiologistikirkon sisäiseen keskuteluun ”peilisoluista”:

Harmaa.Eminenssi kirjoitti 12.06.2005 (176090)...

>Tällaista keskustelua aiheesta muualla:

>http://www.interdisciplines.org/mirror/papers/4/pr

 

RK (176097): Antopavlovistikirkon sisäistä jargoonia. Mutta ERITTÄIN MIELENKIINTOISTA heti en-simmäisessä jutussa, että nimenomaan SOLUTASON ilmiöitä (ehdollistuneita tai muita) EI OLE EDES HAVAITTU muualla kuin Rizzolatti makaki-apinoilla! Ja itse asiassa, kaikki muu tohina huomi-oiden tuon asian ympärillä,SIIHENKÄÄN "HAVAINTOON" EI TAIDA OLLA KAUHEASTI LUOTTAMIS- TA! Arbib myös pulputtaa kovasti matkimisesta apinoilla, ja löytää siihen alkeellisilla apinoilla rudi-mentaarisen ehdottoman (tai leimaus-) refleksinkin, VAIKKA "IHMISEN PEILISOLUTEORIAN" ISÄT Alvin Goldmann ja Vittorio Gallese kategorisesti "KIELTÄVÄT" MATKIMISIMIÖIDEN OLEMASOLON apinoilla ja laajemminkin luonnossa ”:

 

http://keskustelu.skepsis.fi/Message/Message/175827

 

Otetaanpa muutama kommentti tuolta tarkastelun alle.

Michael Arbib: ” 1) Much of the discussion of “mirror neurons” is based on metaphorical discussion of “mirror systems” rather than on analysis of actual neurophysiological data.

Mirror neurons have only been measured in macaque monkeys. Human brain imaging data only provide evidence for mirror systems – i.e., neural regions active both during the execution of a class of actions and during the observation of actions from that class.

A mirror system need not contain mirror neurons, though it is generally assumed that it will. “

 

RK: Kommenttini yllä.

 

“2) My own work with Rizzolatti has suggested an evolutionary path from a mirror system for grasping via a mirror system that supports imitation [not present in more than rudimentary form in monkeys] to a mirror system that can support language [unique to humans]. But this is a theory.   

As far as I know, there is no evidence that mirror neurons are involved in language, imitation, or intersubjectivity. Rather, there is suggestive evidence that mirror systems may be related to these functions. “

RK: On olemassa ja tutkittuna myös ihan muita ja parempia selityksiä kielen tunnistamiselle ja oppimisella, jotka eivät TARVITSE YHTÄÄN SE ENEMPÄÄ ainakaan geneettisiä ”PEILISYSTEEMEITÄ” kuin ”-SOLUJAKAAN”: '

http://keskustelu.skepsis.fi/Message/Message/162827

Kuten Arbibkin tavallista rehellisempänä sosiobiologistina aiheellisesti mainitsee:

 

” In computer science and engineering,simulation involves the ability to predict a trajectory in quan- titative detail. However,if we look at data on mirror neurons, there is no evidence of simulation at such a level of detail. Even worse, to reiterate one of Csibra’s points, many a mirror neuron is only “broadly congruent”. Again, we know there are mirror neurons that fire both when the monkey breaks a peanut and when he hears the sound of a peanut breaking (Kohler et al.,2002). But since the sound gives no information about the manner of breaking, it is unclear what justifies calling this “simulation” rather than just “classification”. If this concern is accepted, one must ask whether the “classification” theory of intersubjectivity loses any essential features of the “simulation” theory. “

 

RK: Olen jossakin hieman erheellisesti maininnut, että ehdollistumisteorian mukainen mielenteoria kuuluu ”peilisolu/systeemiteoreetikkojen” kategoriaan ”simulaatioteoriat” (enemmänkin kuin Gold-mannin kategoriaan ”teoriateoriat”, "theory theories"). Nyt niillä on kuitenkin uusi kategoria ”luokitte-luteoria” (classification theory), johon se vasta istuukin hyvin, esimerkkinä juuri pähkinänkuoren rik-komisprodeduuri, joka aktivoituu myös rikkontuvan pähkinänkuoren aiheuttamasta äänestä,eikä vain sellaisen työn tekemisestä tai katselemisesta! (Itse asiassa siitä on vain yksi kukonaskel symboli-funktioon, että pähkinänkuoren rikkomisääni yhdistetään johonkin kellonkilaukseen, tai SANAAN, joka tuo sen koko ehdollisen refleksin erilaisine variaationeen aktiiviseksi.)

 

” 4) Which leads into the observation that “classification” in the sense of mere “pattern recognition” in no way equals understanding or empathy. “ 

RK: Arbib erehtyy siinä, että tuo refleksin aktivoituminen toiminnan äänestä ei olenkaan liittyisi YM-MÄRTÄMISEEN: se ei vain liity, vaan se suorastan ON sitä! Mutta EMPATIAAN sen ei todellakaan tarvitse liittyä millään tavalla: yhdistetynä muihin toiminalisiin kuvioihin se ”ymmärtäminen” voi ai-heuttaa esimerkisi reaktion, joka ihmisllä vastaisi osapuilleen seuravaa: ”nyt se p..le löysi kumminkin sen mun piilottamani pähkinän, ja rikkoi sen! Turpiin tulee!"

” In other words, it is not the mirror neuron firing itself that is crucial, but rather activity in a widely distributed neural system of which the mirror neurons are part – and it is not even established that mirror neurons are more significant than quasi-mirror neurons in this regard. ”

RK: “Peilisolusta” pidetään kuitenkin kiinni kuin sika limpusta, vaikka sitä EI TARVITA MIHINKÄÄN, ja HAVAINTOKIN niistä on asetettu kyseenalaiseksi!

Lisäksi kehitellään uusia stiiknafuuliota, kuten ”kvasipeilisoluja” (jotka aktivoituvat havaitessa, mutta eivät tehdessä)!

SENKÖ TÄYTISEEN tarvitaan (vielä lisää) tuollaisia VALEKÄSITTEITÄ, se alkuperäinen ”peilisolun” valekäsite oli fysiologisesti tarpeeton, koska jokainen aivokuoren pinnan solu olisi sen mukaan aina-kin jonkin asian ”peilisolu”, mutta tuo ”kvasipeilisolu” on jo LOOGISESTIKIN saman tason "käsite" kuin vanhaa lasten vitsiä lainatakseni ”saippuan nimittäminen ´valeoravaksi´”, koska ”saippualla ja oravalla on yhteinen ominaisuus, että molemmat pääsevät puuhun, paitsi saippua”!

 

” 5) We must distinguish what the macaque data from Parma tell us about mirror neurons from what we tend to claim they tell us. “

 

RK: OLOSUHTEET HUOMIOON OTTAEN: terävästi päätelty…: on pidettävä erillään se, mitä tulok-set kertovat, ja mitä "me" (="sosiobiologistikirkko") HALUAMME USKOA niiden tarkoittavan! Ei käy-nyt niin kuin pikku Kallelle, kun USKONNON opettaja kysyi, että "mikä on ruskea ja karvainen ja hyppii oksalta oksalle". Kalle vastasi, että ”Ensin tuli vähän muuta mieleen, mutta OLOSUHTEET HUOMIOIDEN vastaan, että se on Jeesus-lapsi”. (Vastaavalla odotusarvojen todennäköisyystasolla ovat ehdollistumisteorian (”orava”) ja ”peilisolutoerian” (”Jeesus-lapsi”) edustamat tulkinnat neurofysiologisista kokeista….)

 

” 6) Csibra suggests that “a plausible counter-hypothesis for the role of MNs would be that they are involved in the prediction or anticipation of subsequent — rather than in the simulation of concurrent — actions of the observed individual.”

RK: MITEN tuo on muka “peilisoluteorian” VASTAhypoteesi? Jos siellä ”peilisolussa” on jokin TOI-MINTA koodattuna, niin sehän on sitä juuri ”toimenpiteiden seurantona”, miten se muuten siellä voisi olla? Mutta helvetin paljon yksinkertaisemmin tuollainen selittyy ehdollistumisteorialla ja ILMAN SO-LUTASON KOODAUSTA, koska kullakin niillä osatoiminnoilla voi olla ja on oma refleksikaarensa SA-MASSA "PROSESORISSA", ja niiden välille tarvitaan vain järjestävä yhteys, jotta niistä saadaan ”ko-ko toiminnan refleksikaari” seurantoineen! Tuohon viime mainittuun voi sitten ärsykkenä viitata sana tai vaikka pähkinänkuoren tietynlainen risahdus apinan salavarastolla. Tämä on sitä ehdollisten ref-leksien SYSTEEMISYYTTÄ, että ”ylin” ja ”abstraktein” taso määrää, ja ohjaa hierakisesti niihin alem-piin , perustavampiin, alkupeäisempiin. Sellaista ei esiinny genettisillä erillisillä ehdoTTOMilla reflek-seillä, joissa taas ”alin määrää” . (Esimerkiksi vaikka olisi kuinka herkullisia ruokia ja kuinka kauhea nälkä, mutta sormi pistetään kurkkuun, niin yrjö tulee. ”Vieras esine kurkussa, jota ei voi nielaista” on nimittäin originalinen laukaiseva ärsyke).

 

” 7) Finally, let me note that simulation theorists seldom address the fact that we may be observing others while still going about our own lives. To address this, the simulation theorist must explain how the same neural circuitry could support the simulations of the others at the same time as it supports our own actions, and how it solves the binding problem of keeping the neural representations of agents and actions properly paired as the drama unfolds. “

RK: Tässäkään ei ole ehdollistumisteorian valossa mitään ihmellistä: kaksi eri toimintoa voi hyödyn-tää yhtä aikaa samaa aktivoitua refleksikaarta, siitä on usein vain hyötyä, jos se on muutakin kautta aktiivisena (sanotaan vaikka bändisoitossa tai pariluistelussa, missä on toisella silmällä tai korvalla seurattava naapureiden suoritusta, tuollainen ei oikein automatisoitunesti muuten onnistuisikaan). Mutta jos kaksi henkilöä tekee samaa proseduuria hiukan eri tahtiin ja havainnoi toisiaan, niin sitten voi sekaanusta sattua, esimerkiksi siten, että jäljessä oleva jättää pois jonkin vaiheen ja jatkaa ereh-dykdessä samasta kohdasta missä se toinen suorittaja on. Sillä, ovatko aktivoituvat ilmiöt ”solutason simulaatiota” vai suhteellisesti objektivoitunutta "toimnnan vakiomallia", on olennainen merkitys tukinnan kannalta.

Siitä nämä Gergely Csibran kommentit:

” 1. The existence of "mirror systems" does not tell us anything about simulation. Simulation theories require not only that the same neural substrate be involved in the execution and observation of actions, but also that the actual representations match between these domains.

The claim that mirror neurons "mirror" actions has implicitly (and sometimes explicitly) been exten-ded to "mirror systems" by analogy and terminology.As Arbib notes,there is no evidence supporting this claim. “

RK: Ilman “(Rizzolattin_)mätsäystä” ei ole, tai ei tarvita, “peilisolujakaan”… Nyt tullaan siihen, mikä olisi luokitteluteorian (joka siis sopii ehdollistumisteorian ja kielellisen ajateluteoriankin kanssa, jos sen ei oleteta olevan keenissä) ja ”simulaatioteorian” ero:

 

" 2. Arbib asks "whether the 'classification' theory of intersubjectivity loses any essential features of the 'simulation' theory." Yes, it does - it loses its main point. If an action is 'classified' without simu-lation, then it is understood without simulation, and it is no longer "devoid of meaning" (Rizzolatti et al., 2001), however this meaning is elaborated by further processes.

 

RK:“Simulaatioteorialla” voi pyyhkäistä tiettyä paikkaa ”luokitteluteorian” hyväksi,ja saman tien ”auto- maattisella mielenlukemisella”. Jos esiintyy ”simuloivaa mielenlukemista” se on yhteisen harjoittelun tulos jossakin useamman henkilön työ- tmv. prosessissa. Ja se koskee pelkästään sitä tiettyä, yh-teistä suoritusta edellyttävää prosessia. Seuraavat pykälää kovempien "peisoluteorian" kannatajien "krritiset kommentit" näistä osin kerettiläisistä huomiosta ovat mielenkintoista paljastavaa luettavaa "peilisolutoerian" kannalta...

Pätkäisen tähän tällä kertaa, ja palaan niihin tuonnempana, inshallah... RK ]

 

Gregory Hickok: " The idea that they were exploring was that these were cells that were taking ob-ject shape information and using that to select from a vocabulary of appropriate grasps, the approp-riate grasp gesture for reaching that object. So they were studying this population of cells and as they were swapping the objects in and out of the display case during the experiment they noticed that some of the cells that they were recording from started responding to the experimenter’s own actions. These were cells that responded when the monkey generated movements and as well as when they were observing the experimenter making similar movements. This is basically the response properties of mirror neurons; They respond both during action-execution and also action-observation. That was the basic discovery and the context in which it was made.

The big question became “What are doing?

What’s going on with these cells such as they respond to actions, as well as execution of actions?”

 

Serge: Okay. So from discovering that these very specific cells are activated during action and also during observation of action came the leap that they are responsible for more than that.

 

Gregory: That’s correct. So, in trying to figure out what they were doing, the most obvious interpre-tation or function that these cells could be supporting is direct imitation. So if you have a cell, for example, that responds both during observation and execution you might imagine that that cell allows the animal to directly imitate the actions that it is observing.

That was considered briefly early on after mirror neurons were discovered, but that possibility was ultimately rejected on the basis of the observation that the Macaques don’t seem to imitate like that. They don’t do direct imitation like humans do.

And so that was discarded as a possible interpretation of these cells and they looking for other pos-sible interpretations. There was a theory that had been around since the 1950’s in the speech do-main, my area of research, called the motor theory of speech perception, which held that when we perceive speech sounds, the goal of perceiving speech sound computationally, is not to recover its acoustic form but to recover the gesture of the speaker. That is, the motor plan that generated the sound that you’re listening to. It was very much a motor theory of perception, and mirror neurons kind of looked like that. They were responding during the observation of actions.

The Parma researchers considered the hypothesis that maybe these cells were responsible for action understanding, that’s how the monkeys understand others actions, and the method they proposed was one of simulation.

The logic kind of goes like this: When the monkey generates an action, say a reaching action towards something, it knows what it’s doing, it knows its intentions behind the movement. When it observes another animal generating an action, if it can simulate those movements in its own motor system, then by the same token it will be able to understand other people’s actions. And so you simulate to allow understanding. That’s the basic idea.

 

[RJK: Tämä virheellinen päättely kantaa sisällään ensinnäkin olemukseltaan LOOGISTA Damasion virhettä (joka palautuu ennen Pavlovin ehdollistumisteoriaa esitettyyn James-Lange-teoriaan), jonka mukaan "tietoisuus on kuudes aisti, joka aistii muiden aistien aistimuksia": tietoisuus (tietoinen tajunta) siis SEURAISI NEUROTOIMINTAA eikä aiheuttaisi sitä.

Virhe on nimenomaan looginen siksi, että "Uusi Kuudes Aisti(n)" SISÄLTÄÄ PILKULLEEN SAMAT ONTOLOGISET JA MUUT ONGELMAT KUIN NE VIISI "VANHAAKIN" AISTIA, EIKÄ SE SIIS RATKAISE TUTKIMUSONGELMIA, vaan pelkästään siirtelee niitä toiseen, entistäkin ratkaisemattomampaan paikkaan.

https://hameemmias.vuodatus.net/lue/2014/08/yhteenvedon-paikka-antonio-damasion-biologismista-2004
 

Yhteenvedon paikka Antonio Damasion biologismista... (2004)

 

Spinozaa_etsim%C3%A4ss%C3%A4.jpg

 

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/136367?page=1#136367

" Aamulehdessä 14.03.04 oli Tampereen teknillisen yliopiston fysiikan dosentin Jouko Niemisen arvostelu portugalilaissyntyisen mutta nykyisin USA:ssa tutkijana ja kirjailija-na vaikuttavan Antonio Damasion kirjasta "Spinozaa etsimässä - ilo ja suru ja tuntevat aivot".

 

Screenshot-2018-5-10%20Jouko%20Nieminen.
Dosentti Joko Nieminen

Kirjoittaja edustaa juuri sitä kohderyhmää tyypillisimmillään, jolle esimerkiksi Antonio Damasion, Steven Pinkerin tai vaikkapa vain suomalaisen sosiologin Ullica Segerstråhlen, näiden "Euroo-passa vainottujen", mutta sitten USA:ssa "tieteellisen" uran luoneiden, kirjoittelu on tarkoitettu...

Omana yhteenvetonani toistan ne moneen kertaan tälläkin palstalla esiintyneet syyt, joiden takia Da-masion tietoisuusteoria EI OLE tieteellisten periaatteiden mukainen pätevä teoria, eikä se siten nykyisen tieteellisen maailmankuvan mukaan voi olla myöskään tosi teoria, ainakaan kokonaisuutena. (Yksittäisiä oikeita oivalluksia tai havaintoja siihen saattaa sisältyä.)

 

1. Damasion teoria tietoisuudesta "kuudentena aistina",joka (ikään kuin ulkoisena havaitsijana) aistii muiden aistinten tuottaman datan käsittelyä aivoissa, eli että "havainnoimme havainto-jamme",on karkeasti LOOGISESTI virheellinen teoria, joka EI SELITÄ MITÄÄN, vaan siirtää pelkästään tietoisuuden ongel-man uuteen paikkaan,sillä aivan sama ongelma liittyy tuon "muita aisteja havainnoivan aistin" tietoisuuspuoleen kuin niiden alkuperäistenkin aistien!

 

Ja pahempaa: jos alun perin oli JOKIN MAHDOLLISUUS havainnoida korrelaatiota esimerkiksi aisti-miin tulevien ulkoisten signaalien ja esimerkiksi aivokuoren aktivaatiotason välillä, ja yrittää niistä ve-tää johtopäätöksiä, niin nyt PERIAATTEELLINENKIN kokeellinen tsekkausmahdollisuus on men-nyttä, kun ilmeisesti kyse olisi "aivoalueiden välisistä" havaintokorrelaatiosta, joista emme edes tiedä, mitkä alueet ovat kyseessä (emme varsinkaan se uuden "aistimen" osalta)!

Tuo karkea virhe on puhtaasti looginen ja filosofinen, sen havaitsemiseen ei tarvita MINKÄÄN-LAISIA neuro- eikä muun psykologian tietoja. Se on tuossa suhteessa vähän niin kuin karkea mate-maattinen määrittelyvirhe minkä tahansa konkreettisen "teorian" premisseissä: tutkimusongelmia ei ratkaista, vaan ne kasataan eräälaiseen ("kantilaiseen") "das Ding an sich"-pisteeseen, jossa niitä EI PERIAATEESSAKAAN voida tutkia eikä ratkaista.

 

Olli Lagerspetz: Onko tietoisuus elimistön organisaatiotaso?

https://netn.fi/sites/www.netn.fi/files/netn991-02.pdf

Kritiikki pätee myös Damasion niin ikään olettamiin "(aineettomiin) mielen karttoihin", jollaisiin kuu-lemma aistimuksessa kaiken aikaa "kehon kulloistakin tilaa ("lihaa", "fyiikkaa")verrataan": ei siinä to-dellakaan RATKAISTA ideaalisen ongelmaa, vaan siirretään se pllkästään toiseen, vieläkin vaikeam-min tutkittavaan paikkaan (aivan kuten "Jumalakin" selittää selitämätöntä vieläkin selittämättömämmällä")!

2. Damasio nojautuu ns.James-Lange hypoteesiin,jonka mukaan "tunne on havainto elimistön tilasta". Hypoteesi on vakuuttavasti osoitettu vääräksi, sillä tunteella on aina KOHDE, ja sen ytimessä on tuota kohdetta koskeva tieto, jolla sitten sattuu olemaan jonkinlainen biokemi-allinen "glorifionti" tai päin vastoin "aversifionti", vastenmielistävä tuntemus.

On ollut ainakin sata vuotta tunnettu tosiasia, että tuollainen glorifiointi tai aversifiointi voidaan saada aikaan kemiallisestikin esimerkiksi huumeilla tai sähköisestikin laukaisemalla vaikka nauru (tai orkku) selkäytimstä, mutta Damasio esittää tällaiset omina uusina "mullistavina" tuloksinaan, jotka "todista-vat", että muka "ensin on reaktio" ja sitten vasta tunne, vaikka (sinänsä olemuksellisesti ehdollistu-mislakien mukaisesti kahdensuuntainen) prosessi on noissa esimerkeissä nimenomaisesti pistämällä pistetty pelaamaan tavanomaiseen nähden päinvastaiseen suuntaan!

Damasio on sekoitanut "tunteen" "tuntumaan" (esimerkiksi voimistelijan oman jalan asennosta), joka on todellakin aistimus elimistön tilasta, mutta jolla ei sitten ole paljoa tekemistä ilojen ja vihojen ja rakkauksien varsinaisen olemuksen kanssa.

Ohessa tunnetun englantilais-amerikkalaisen filosofin Colin McGinnin niittaus niin James-Lange-teorialle kuin itse Damasion kirjallekin:

keskustelu.skepsis.fi/html/KeskusteluViesti.asp?ViestiID=117041

 

3. Damasio esiintyy niin kuin ei olisi ikinä kuullut mitään ns. korkeimpien psyykkisten toiminto-jen nykyaikaisen tieteellisen maailmankuvan mukaisesta selittämisestä kielellisen ajatteluto-rian avulla eikä myöskään sen biologisena perustana olevasta EHDOLLISTEN REFLEKSIEN järjestelmästä.

Hänen teoriansa kuuluu siis ns. Anti-Pavlov-teorioiden kategoriaan, jotka ovat nykyisen tieteellisen ihmiskuvan mukaan humpuukia, sillä ehdollistumislait on kyllä miljoonaan kertaan osoitettu kokeelli-sesti todellisiksi ja sivuuttamattomiksi esimerkiksi juuri tietoisuusilmiöiden selittämisessä.

http://keskustelu.skepsis.fi/Message/Message/361268

http://www.nytimes.com/2003/02/23/books/fear-factor.html?pagewanted=all

 

Mutta sitten kirjoituksen yksityiskohtaiseen analyysiin (kirjoitan sen saman tien nettiin kuin tiedostoonkin, ja nyt voitte sitten oikaista virheet, jos osaatte...):

 

Jouko Nieminen:

Tunteiden biologiassa humanismi kohtaa luonnontieteet

2004-03-14

Antonio Damasio: Spinozaa etsimässä - ilo suru ja tuntevat aivot

 

Ja lopuksi: tutkiessaan tuota "toisten tiedostamisen mallintamista" ihmisapinoilla, silloinen peilisolu-mies Michael Tomasello todisti, että NIIN EI OLE: vain ihmisellä on jaettu intentio (johon siis tuolla peilisolulörötyksessäkin "lähteenä" täysin väärin tietysti viitataan!

 

Tämä olisi pitänyt arvata jo seuraavasta seikasta: APINOILLA EI OLE SILMÄNVALKUAISIA! Ne ni-menomaan EIVÄT NÄE, minne naapuri katsoo! SIITÄ on ollut NIILLE ENEMÄÄN EVOLUTIONAA-RISTA HYÖTYÄ, siis "aikeiden salaamisesta", kuin niiden paljastamisesta kuten ihmisillä! Simapans-si pystyy kääntämään katsettaan 120 astetta päätään liikuttamatta ilman että ulospäin näkyy mitään ilman erikoislaitteita, jollaisilla Tomasello tutki niiden katseiden suuntaa.

MILLOIN ne valkuaiset ilmaantuivat, onnistuneen jaetun intuition ehdoton edellytys?

Tässä yksi, taiteilijan teoria:

http://jatkumo.net/index.php?topic=2096.msg175234#...

Tämän kuvan taiteilija on mitä suurimmalla todennäköisyydellä olettanut Ardipithcus ramiduksella (kuva), oletetulla vesiapinalla, olleen jaettu intentio (vaikka sillä edelleen mitä todennäköisimmin ei olut sialiinimutaatiota päätellen "pienistä" aivoista).Ardipitehecuksen seuraaja oli (luultavasti) Austra- lopithecus Africanus, ensimmäinen juokseva ihmisapina ja ensimmäinen ihmisen tapaan juokseva laji, täysin kuivanmaan elävä. (Jos sillä ei ollut sialiinimutaatiota, se juoksi paljon lujempaa kuin kuin jos oli. Periaatteessa ihminen olisi saatanut olla myös noiden risteytys: ne olivat kuitenkin lähisukulaisia.)


 


 

 

 

" Serge: So, in a way, the part in there is not just that its possible to simulate in order to understand, the question and some of what you discuss in your book is about the nature of understanding.

Is how we understand sayings based on basically imitating the movement?

And so it raises the question of how we know what we know, and how we understand what we understand, and how we attach meaning to things.

 

Gregory: That’s exactly right. The big problem with this idea is that the movements themselves contain meaningful information, or that by observing or simulating the actions it will automatically tell us what the meaning of those actions is.

If you think about it for a little while,it’s obvious that it’s not the case and there’s several reasons why if we look closely. For example, if I reach for a pitcher and tip it over so that it pours water out into a cup that action can mean many different things depending on the context. So if there’s no water in the pitcher, it’s just a tilting motion, it doesn’t really do anything, it’s not pouring. If there’s water in there then we can think of it as pouring. If we think about it from the perspective of the cup then it’s filling. The movements are identical, so you can generate very similar or identical motor patters and achieve the same goal.

The movements really don’t define the meaning, they’re actually quite ambiguous. It really depends on the context and a lot of the mirror neuron experiments demonstrated this, that the same movement that the monkey observed gave rise to mirror neuron activity not depending on the movement but depending on the context, and that’s in the mirror neuron literature. It’s not the movements themselves that are defining it.

 

Serge: So the interesting part then is that it is more complex, that the movement itself is one source of information and the processing involves many sources of information.

 

Gregory: Right. In order to understand something you need all this additional context and the movement is only a small part of it. It may be that, perceptually, it’s an important part to process that movement, but it doesn’t mean that simulating that movement in your own body is going to tell you much of anything.

We know empirically that in individuals that don’t have the ability to move, they seem to be able to understand the world quite well. We all can understand action that we have never performed previously, say a reverse slamdunk in a basketball game for example. Not many of us can do that, but we can understand it quite well. Other animals that have movements that we can’t possibly generate we can still understand, so flying or slithering or things like that. And there’s good evolutionary reasons why we would want to understand the actions of other animals, because sometimes they’re predators and we want to know what they’re up to. Sometimes they’re prey, and we want to predict what they might do so that we can catch them better. There’s lots of reasons why we should have neural systems that allow us to understand the actions of others without having to simulate these actions.

 

Serge: So, in other words what you’re saying is that mirror neurons are certainly a source of information, but they’re not the source and certainly not the source of meaning.

 

Gregory: Well, not quite. The way I view mirror neurons is they’re essentially important for motor control just like these cells in F5 are important for using sensory information about object shape to guide action selection. I see mirror neurons as doing exactly the same thing. Instead of object shape they’re using action, they’re using dynamic information about movement in order to guide responses. Generally, you can understand that the actions of other animals or people are important for selecting our own actions. If I thrust my hand out towards you when we first meet you’ll likely respond with a similar gesture to shake hands. If I do something else like throw a punch, you’re going to want to select a different action, a blocking or ducking action for example. Presumably, this is very important in the monkey world as well, and I think it’s that action selection function that mirror neurons are actually doing. I think the understanding is coming from different circuits, it’s coming from sensory circuits that are involved in recognizing actions, connecting them to meaning, integrating them with context, and all sorts of things. The involvement of the motor system is just to select actions that are appropriate to the understanding we get from other systems.

 

Serge: So is there maybe a hierarchy there of some things, some situations where there’s more instinctual reactions, and some cases where there’s more involved, more processed reactions?

 

Gregory: Certainly it’s the case that we have reflex-like responses. Like I said, if I threw a punch at you, reflexively you would want to duck, or block,or do something like that. I think one way to think about it is in terms of general brain organization into what’s often been referred to as dorsal and ventral streams, sensory streams.The dorsal stream is thought to be involved in sensory-motor in-tegration. This is a parietal-frontal circuit that is taking sensory information and is using that to guide actions and that can be thought of as more of a reflexive, online, immediate system. That’s the sys-tem that mirror neurons are apart of. And then there’s a ventral stream circuit that’s more involved in recognizing what is going in the sensory environment. You can think of it as taking sensory infor-mation and trying to link it up to medial-temporal lobe structures involved in memory, episodic memory, all sorts of things like that.

So you can think of it as hierarchical in the sense that you have in some sense a lower level motor circuit that can respond reflexively taking information from a more cognitive or higher level concep-tual system that’s involved in recognizing, attaching meaning, attaching emotional relevance to information that’s in the environment. I think it is kind of helpful to think about organization of these circuits in terms of that kind of hierarchy and placing mirror neurons and other sensory motor circuits within one stream. It’s not particularly involved in recognition, but it’s involved in taking action.

 

Serge: And involved in taking action, but there is a difference anyway in the action that’s being taken in terms of the context. So that’s where you would make the difference, say, between the action you take at first and the action you take once more you’ve had time to process at a higher level?

 

Gregory: Yeah, certainly it’s the case that some things are very reflexive. I mean, generally you can think of the nervous system as being layers of control, so at the lowest level you have things like spinal reflexes which will get triggered automatically, but on top of that you have other circuits that are built to modulate that low-level reflexive response, because we don’t want to always respond reflexively. Sometimes, depending on the situation, we may not want to release that hot pan knowing that it might make more of a mess, knowing that if we drop it than if we quickly set it down or do something else. So yes, it’s always the case that we have some sort of higher level of control over these things.

We can decide after observing an action and understanding it whether we want to respond to it or not. And, of course, there are degrees of how reflexive our responses are. But I think the important thing is that mirror neurons are essentially in a motor control circuit, that they are not the basis for understanding, they’re kind of the endpoint for understanding.

They respond after the understanding takes place, which is very much characteristic of the way that these cells respond in monkeys. So, for example, in one experiment the researchers placed an object behind a screen so that the monkey couldn’t see it anymore and then reached for it and mirror neurons fired.

It is interesting that mirror neurons will not fire if the experimenter is reaching for nothing or just pantomiming a reach. That object has to be there in order for that to happen. It doesn’t physically have to be there in the sense that you could put it behind a screen that is physically in view, you can put it behind a screen, the monkey knows it’s there, and it will respond to it even though it can’t see it.

So Serge: I just want to interrupt you here, because as you’re talking you’re clarifying something for me. When you first said, at the beginning of your answer that something comes first, in a way takes me in a little bit of a loop. I think of the word understanding as referring to more conceptual, abstract understanding, as if in a way rational thinking preceded action. And as you’re talking more about this it’s actually something different that’s coming up. It is not understanding as some kind of abstract reasoning, but as having a context so that reaching is not a gesture in and of itself, but that is reaching for something. And it’s that mix of a gesture, and a goal, and a total context that is what you call understanding. Is that what you’re talking about?

 

Gregory: Yeah, I mean if we go back to the experiments that show when mirror neurons fire and when they don’t, they will fire if there is an object to be grasped. They won’t fire is there’s not an object to be grasped, and that’s going to depend on the context, the non-motoric context. And so there’s got to be some level of understanding of what the goal of that actual action is going to be before the mirror neurons will even fire. The typical interpretation out there in terms of mirror neu-rons is that they fire to tell you what the goal is. If they have to know what the goal is in order to fire then some level of understanding needs to be taking place before this circuit gets recruited. And so yes, I do think that there is some sort of a contextual understanding of what the goal of a reach is and what actions that might map onto in the monkey before these cells will actually fire.

 

Serge: So then in a way even at the level of something relatively basic like mirror neurons we’re still in a system where it’s not just sensory is pure stimulus and pure stimulus gives the reaction. Even in that case we have a more complex process where we are attaching context and processing information before the reaction happens.

 

Gregory: Sure, yeah, and just think of your everyday life. If we were completely reflexive, every cup, every object that you looked at you would reflexively reach for. Or, anyone who reached out for something or did something, you would mirror it or perform a similar action.

 

Serge: When you say this, actually it’s an interesting point. One of these reasons that the concept of mirror neurons caught on so well with psychotherapists is that in our everyday life seeing clients we catch ourselves “mirroring” the movements, the hand gestures, the body language, the moving of hands, the moving of legs of our clients, and vice versa. So in that way, it’s very tempting to jump into it and say “Oh, this must be mirror neurons.”

 

Gregory: Yes, that is a documented phenomenon, it’s known as the Chameleon Effect, and it’s something that I discuss in the book in the chapter on imitation. Humans do it. Macaques don’t do it, which is kind of interesting because Macaques have mirror neurons and they have the system that presumably would allow this, and yet they don’t do it.



[RK: Siis makaienkaan "peilineuroneista" (että ne eivät ole esimerkiksi VIEREISIÄ jonkin tikapuumallisen refleksikaaren mielessä) EI OLE LOPULTAKAAN NÄYTTÖÄ...

Hickok painottaa nyt sitä, että VAIKKA OLISI, niillä, niiden luonnonhistoriallisilla jatkeilla, EI olisi tekemistä uhmisentajunnan kanssa.]



And so it’s something beyond mirror neurons that’s actually allowing this ability.

What’s it for?

It seems to serve a social function.

These sorts of things have been demonstrated experimentally in work that has people perform an irrelevant task in the company of a confederate to the experiment who’s generating some behaviors. When the confederate scratches their head the experimental subject will tend to scratch their head. The interpretation of this Chameleon Effect is that it is serving a social function to essentially provide social acceptance, or provide in-group status, or something like that. It’s interesting that humans tend not to imitate or mirror people that they don’t like or don’t identify with, so it is a kind of unconscious imitation, mirroring if you want to call it that, but it is not a dumb process, it’s not a reflexive process.

Presumably what’s happening, as is the case with other kinds of mirroring or motor control, is that there is some sort of higher-level circuit that is controlling or enabling this process to take place. It’s that process that we want to understand to know what’s happening with this kind of Chameleon Effect mirroring.

We need to think about what this higher-level circuit is doing such that it can activate the lower-level mirror-like circuit.

 

Serge: Right. And so, the image of mirror is the same that, say, can be used in contemplative ap-proaches to life; that wish that our minds were like a mirror that simply reflects the world as it is, and with some training and skill we can eliminate what gets in the way of that and have the purity of out-side experience. What you’re reinforcing and what you’re saying is that actually everything in our brain is designed to interpret experience as opposed to reflect it.

 

Gregory: Well, if we look to perceptual science,perceptual neuroscience - you’re talking about things that are way beyond my ability to comprehend myself, fairly abstract things - but if we ground those things in perceptual science, we know as a matter of fact that we don’t simply perceive or resonate with the world. Our brain actively constructs a representation of what the world looks like. If that’s true, even at the perceptual level, even in perceiving cups and things like that, if you scale up to human experience or more complicated situations, that with more force is a construction of our mind in terms of how it interprets the world.

Serge: And so,in a way,how does this bring us,in terms of concept of how we know what we know, how we conceptualize what we experience, and that whole concept and discussion you have in the book about embodied experience, embodied cognition? On the one hand, you know, there is it seems like we must have evolved in way that we developed abilities to deal with the world that were more complex, but based on simpler processes. On the other hand, such possible mechanisms as mirror neurons appear flawed as explanations of it.

Gregory: Yeah,the embodied cognition movement is an interesting thing.I think there are parts of it that are quite accurate and that are reasonable, so one of the things I like about it is that the move-ment tries to take complicated cognitive processes, and cognitive is kind of a loaded term as I talk about in the book, but complicated processes like categorization, or problem sol- ving, or decision making, things like that, try to think about how these might be done in terms of lower level circuits and sensory-motor circuits. I think that’s an interesting research direction to take. Where I think the program has gone wrong is this notion of simulating. Basically the idea is the way we think about, say, cats or dogs or something, is we simulate the sensory expe- rience, and that’s often taken as an explanation of how it’s done. “Oh, we just simulate it, the concept of cat in our sensory-motor systems, or whatever,” and that’s actually how we understand it, but this doesn’t tell us much at all.

Simulation is just a term for, basically, information processing,and what we really want to do is figure out what happens in the initial process. So to say that we simulate our experiences with cats in order to understand them, that’s fine, but then we want to know “What is this experience with cats?” How is it coded in our sensory-motor systems or whatever, to give rise to our un- derstanding in the first place? To say that we simulate it doesn’t really help, it kind of renames the problem, essentially.

Serge: Just like calling it a process, essentially.

Gregory: Yeah, that’s right. And so the embodied program is interesting, I but I think as a replace-ment for traditional cognitive psychology it has failed. It doesn’t really change much of anything except to look for lower level processes in the brain, which themselves are quite abstract in terms of trying to explain some of these higher-level behaviors.

Serge: So the flaw, as you see it, is that it tries to provide an explanation for what happens, but in a way that doesn’t match the information we have about how it happens.

Gregory: That’s right. There’s lot’s of empirical evidence that I discuss in the book showing that essentially you don’t need a motor system in order to understand actions. I go through that in the speech case, which is a domain that mirror neurons were first generalized to in humans. Speech was really the human connection between monkey mirror neurons and what’s happening in humans because we have a lot more data on that. There was this motor theory about speech perception that was out there; incidentally, that theory was rejected by speech and language scientists before mirror neurons were discovered, so it’s kind of a poor analogy to use to help interpret mirror neurons since the theory was essentially dead. But, there’s evidence, for example,of individuals with cerebral palsy who can’t control their speech muscles. They had never spoken yet could nonetheless understand speech quite well. There’s examples from people who can’t move and can understand actions quite well, for example in apraxia or congenital disorders like cerebral palsy, or ALS, or other things like that there are examples of people who can’t generate emotional facial expressions. This is Mobius Syndrome.They can nonetheless understand emotional facial expressions as well as anybody else.

So there’s example after example like this that show that you don’t need the ability to move in order to understand, so this explanation is just empirically false.

 

Serge: Right, right. So, it’s not necessarily that we are replicating the movement in order to under-stand it, but that maybe the information about movement is accessed by that part of our brain, our mind, that processes information that processes representations and influences our pre-motor information?

 

Gregory: Yeah, I mean there’s another area that isn’t discussed much in the mirror neuron literature that’s ben discovered in Macaque monkeys as well as in humans, posterior (spoken at 28:30) supe-rior temporal sulcus, which seems to respond quite well to the perception of all sorts of movements, eye gaze, and all sorts of interesting interactions between eye gaze and observed movements, and this sort of thing. This region is probably the hub for understanding actions. In humans it’s involved in biological motion perception, so it’s a big candidate for an area that’s processing this sort of infor-mation and relating it to contextual information, to long-term memories, to all these sortsof things. For actions that are recognized in this way and that are appropriate for generating a response, be-cause not everything we observe is selected for response, then this information can be the sensory-motor parietal-motor parietal-frontal circuits can then be mapped onto motor circuits for action selection that may or may not be mirror related. So, if I thrust my hand out to shake your hand then you’re going to generate a mirror movement, but if, like I said, throw a punch, you don’t want to ge-nerate a mirror movement in that case. And so, I see these mirror neurons as part of a much broa-der sensory-motor circuit only some of which are coding mirror-like movements. There are plenty of others that code anti-mirror movements, and those were actually discovered alongside mirror neu-rons in Macaque monkeys in the original experiments, but these were not discussed theoretically.

 

Serge: Great. So Greg,is there something else you might want to say to conclude this conversation?

 

Gregory: Well,there’s one other topic that I dealt with in the book that might be of interest, and that’s autism, because the Broken Mirror Theory of Autism is quite popular, and like many theories of autism it assumes that something is broken, that these individuals have a lack of empathy, or an inability to empathize or read other people’s minds, things like that. "

https://www.theguardian.com/science/neurophilosophy/2013/aug/23/mirror-neurons

" Reflecting on mirror neurons

The discovery of mirror neurons has been touted as one of the most important of modern neuroscience, but what exactly are these cells, and should you believe the hype?

@mocost

Fri 23 Aug 2013 19.20 BST First published on Fri 23 Aug 2013 19.20 BST

Broken mirror

Mirror neurons have been used to explain everything from language acquisition to autism. Photograph: Alamy







HIckok: " But, there’s another possibility in that they’re hypersensitive and that can lead to avoidance behavior, which can then affect their ability when you assess them to show empathy. This is not because they can’t do it, but because they’re avoiding it.

 

Serge: They’re flooded and therefore avoided.

 

Gregory: Exactly. So there’s lots of reasons to think that a mirror neuron hypothesis and even just a deficit hypothesis for autism is valid and there’s lots of data suggesting that we should be conside-ring alternative possibilities. So that’s another thing that was discussed that may be of some interest to people.

 

Serge: Great, great. Well, thanks Greg.

Gregory: Sure, thank you.

This conversation was transcribed by Michael Fiorini. "

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NäytäPiilota kommentit (9 kommenttia)

Käyttäjän grohn kuva
Lauri Gröhn

Ns. aivotutkijat kirjoittavat sujuvasti mistä tahansa. Esimerkkinä Minna Huotilainen:

”Ihmisillä näitä peilisoluja on monessa kohtaa aivoja, muun muassa otsalohkon liikealueilla ja ohimolohkossa. Pieni osa niistä toimii näön lisäksi myös kuuloaistimusten perusteella.

Peilisolut ovat varsin fiksu kuvastin, enemmän kuin imitoijia. Ne täydentävät havaintoa, jos osa tapahtumasta jää näkemättä, ja reagoivat siihen, mikä on vasta tapahtumaisillaan. Vauva tosin joutuu odottamaan noin vuoden ikään asti ennen kuin oppii reagoimaan muiden liikkeisiin ennakoiden.

Tutkijat selvittelevät parhaillaan peilisolujen vaikutusta lajihistoriaamme. Olisiko jopa kieli syntynyt peilausmekanismin kautta? Niin kutsuttu puheen havaitsemisen motorinen teoria esittää, että ihminen tunnistaa puheen pikemminkin sitä motorisesti simuloimalla kuin akustisten piirteiden perusteella.”

Ja sovellettu psykologiakin sujuu kuin vettä vaan:
http://grohn.vapaavuoro.uusisuomi.fi/kulttuuri/256...

Matti Begströmin inkarnaatio?

Risto Koivula

Harrrmin paikka, että tuo Shanghain yliopiston kiinalainen niitti peilineuroniteorialle ja erityisesti "peilineuroniautismille on on kiinankielinen!
Siinä on kuitenkin English Summary ja lähdeluettelo lähteiden alkukielellä.

http://journal.psych.ac.cn/xlkxjz/EN/10.3724/SP.J....

The myth of broken mirror theory of autism: Origins, problems and prospects

PAN Wei 1; CHEN Wei 2,3; WANG Yin 4; SHAN Chun-lei 5

(1 School of Rehabilitation Science, Nanjing Normal University of Special Education, Nanjing 210038, China)
(2 Center for the Study of Language and Cognition, Zhejiang University, Hangzhou 310028, China)
(3 Department of Psychology, Shaoxing University, Shaoxing 312000, China)
(4 School of Psychology, New York University, New York 10003, USA) (5 School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China)

Abstract

Autism are characterized by difficulties in reciprocal social interaction, verbal and non-verbal communication, and repetitive activities and narrow interests. A core diagnostic criterion of autism is abnormal implicit social cognition. Based on the assumption that mirror neuron sys- tem is the unified neural basis of implicit social processes, the “broken mirror” theory attributes most social deficits in autism to impairments in mirror neuron system, leading to the issues with social skills, imitation, empathy, and theory of mind seen in people with autism. However, after a decade of extensive examination and verification, this theory has been facing increasing challenges from behavioral, neuroscientific and clinical research. This paper outlines literatures examining the unified role of mirror neuron system for implicit social cognition, and systemati- cally review studies testing a global dysfunction of the mirror system in autism. We conclude that mirror neuron system plays a sufficient but not necessary role for implicit social cognition and very few evidence supports that an all-or-nothing problem with the mirror neuron system can underlie autism. The implications and future research directions are also discussed.

http://journal.psych.ac.cn/xlkxjz/EN/10.3724/SP.J....

1 引言
自闭症(autism), 又称孤独症, 现与阿斯伯格
综合征(Asperger syndrome) 、儿童瓦解综合征
(childhood disintegrative disorder)以及未分类广泛
性发展障碍(pervasive developmental disorder not
otherwise specified)统称为自闭症谱系障碍(autism
spectrum disorder)。作为病因未明的神经发育疾病
(neurodevelopmental disorders), 其主要症状为在
各种场合出现持久的社会沟通和交往障碍(涉及
社会情感互动缺陷、非语言行为交流缺陷、发展
维持和理解人际关系的缺陷), 伴随狭隘的兴趣、
刻板的重复行为或活动模式(涉及刻板或重复躯
体运动、高度受限的固定兴趣、感觉输入的过度

***

Lähteet.

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Cattaneo, L., Fabbri-Destro, M., Boria, S., Pieraccini, C., Monti, A., Cossu, G., & Rizzolatti G. (2007). Impairment of actions chains in autism and its possible role in intention understanding. Proceedings of the National Academy of Sciences of the United States of America, 104, 17825–17830.

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Risto Koivula

Tässä luettelossa on sekä peilisoluteorian kovimpia ja tunnetuimompia kannattajia kuten Rizzolatti, Fogassi, Gallese (Parma) ja Ramachandran (San Diego). Fundamentalistien mukaan peilisolussa "sille solulle ominainen ajatus" "luetaan geenistä": ("geeni ilmenee", expresses...). Itse tuo aivopieru on vanhempi, Eric Kandelilta, ja perustuu merietana- tutkimuksille (Aplysia). Tuosta ryhmästä myös puuttuu paljon tunnetuintakin aktiiviväkeä, mm. kaikki suomalaiset ja Harvardissa kärytetty Marc Hauser.

https://hameemmias.vuodatus.net/lue/2015/02/marc-h...

Siellä on myös fundamentaalisimmat vastustajat kuten Alfonso Caramazza (Harvard, Hauserin seuraaja muuten, tapellut Italiassa Rizzolattia vastaan), ja Ilan Dinstein (Tel Aviv), jotka sanovat, että minkään formaaleimman ja epätoiminnallisimmankaan määritelmän mukaisisia "peilineuroja" ei ole lainkaan, vaan havaitessa purkavat aina kokonaan eri neuronit varaustaan kuin suoritettaessa.

Toiset, mm. Gregory Hickok ja Vladimir Kosonogov (Murcia, Espanja), ovat sitä mieltä, että kaikki mahdolliset "peilisolut", jos sellaisia formaalisti on sekä havaintoon että suorituk- seen liittyen varauksensa purkavina, ovat effenttejä (ex-ferenttejä, vieviä) "SUORITUS- PUOLEN" neuroneita, joden viesti ei havainnossa kuitenkaan välity teoksi (mikä on ehkä synaptisen ohjauksen ilmiö),EIKÄ NIILLÄ OLE TEKEMISTÄ YMMÄRTÄMISEN KANSSA. Pannaan tästä nyt vielä toinenkin linkki, vaikka koko juttu käsittelee läheinnä tätä.

https://link.springer.com/article/10.1007/s11062-0...

Löysempää peilineuronilinjaa edustavat opittujen peilineuronien teoreetikot kuten Iacoboni ja Kaysers, joille "peilisolut" ovat Pavlovin klassisten ehdollisten refleksien (joissa reaktio-osa geneettinen, kuten koiran kuolaus muista ärsykkeitä kuin verenhajusta, josta refleksi on ehdoton) genneetisten reaktio-osien sijaintipaikkoja,joihin yhteydet muodostuvat toimin- nassa. Tämä teoria johtaa lopulta samoihin isompiin hölmöyksiin kuin fundamentaalinen peilineuroniteoriakin.

http://www.kaapeli.fi/~euvkr/6-05.pdf

Risto Koivula

Pistin tässä vähän Google Translatella konekäännöstä tuosta Shnghain yliopiston kiinankielisestä jutusta parin vuoden takaa, joka lienee vasta nyttemmin tullut nettiin.

https://hameemmias.vuodatus.net/lue/2018/07/peilin...

Myths of Autism Broken Mirror Theory: Origin, Problems and Prospects

https://hameemmias.vuodatus.net/lue/2018/07/shangh...

"Peilineurooniautismista"...

Risto Koivula

http://tyynekuusela.puheenvuoro.uusisuomi.fi/11200...

" Päätöksenteon magneettikuvantaminen" on huijausta

22.7.2012 01:11 R. Tyyne Kuusela 5 kommenttia

Oppimisen ihmisellä aiheuttamista muutoksista aivojen harmaassa ja valkeassa aineessa uusi seikkaperäinen esitys:

www.nature.com/neuro/journal/v15/n4/full/nn.3045.h...

" Plasticity in gray and white: neuroimaging changes in brain structure during learning

Robert J Zatorre, R Douglas Fields & Heidi Johansen-Berg

Nature Neuroscience 15, 528–536(2012) doi:10.1038/nn.3045

Published online 18 March 2012

Abstract

Human brain imaging has identified structural changes in gray and white matter that occur with learning. However, ascribing imaging measures to underlying cellular and molecular events is challenging. Here we review human neuroimaging findings of structural plasticity and then discuss cellular and molecular level changes that could underlie observed imaging effects. Greater dialog between researchers in these different fields would help to facilitate cross-talk between cellular and systems level explanations of how learning sculpts brain structure.

The brain is the source of behavior, but in turn it is modified by the behaviors it produces. This dynamic loop between brain structure and brain function is at the root of the neural basis of cognition, learning and plasticity. The concept that brain structure can be modified by experience is not new, but it has proven difficult to address experimentally. Recent developments in structural brain imaging techniques (Figure 1, Box 1), particularly magnetic resonance imaging (MRI), are now propelling such studies to the forefront of human cognitive neuroscience.

A connection between brain function and brain anatomy might be expected because neural information processing depends on the size, configuration and arrangement of individual neurons; on the number and type of local synaptic connections they make; on the way that they are interconnected to distant neuronal populations; and on properties of non-neuronal cells, such as glia. Neuroimaging evidence, reviewed below, shows both differences in structural features among individuals and the relevant functions that these structures subserve, and changes in structural features when long-term neural activity patterns are changed by experience.

However, existing neuroimaging techniques cannot directly inform us about the underlying cellular events mediating the observed effects. Moreover, phenomena visible with MRI are likely never the result of a single process happening independently, but probably involve many coordinated structural changes involving various cell types. Conversely, neuroimaging techniques offer certain advantages, as they can be repeatedly performed in the same individual and provide whole-brain measures of brain structure and function. Contemporary neural models of cognition stress the idea of interacting functional networks; it is therefore logical to search for network-level patterns in anatomical structures as well. Recent studies examining inter-regional correlations of cortical thickness reveal that gray matter anatomical networks parallel functional organizational patterns1, that they are modified during development2 and that they are sensitive to training3. The ability provided by macrostructural imaging methods to understand both function and anatomy in terms of regional interactions is likely to grow in importance and can also help to create hypotheses to which cellular and molecular probes can be applied.

Here we consider findings that have emerged from the human anatomical neuroimaging literature, discuss the questions raised by them and propose some possible microstructural mechanisms that could underlie the observed macrostructural findings.

Brain anatomy and cognitive specialization

Many studies have exploited anatomical imaging to reveal group differences that reflect skill, knowledge or expertise. Among the first was the demonstration of larger posterior hippocampal volume in expert taxi drivers4. The obvious implication was that this finding represents experience-dependent plasticity of a structure involved in spatial navigation, a conclusion supported by a correlation between years of experience and hippocampal volume in this population.

Related findings have been reported in many other special populations. Musicians consistently show greater gray matter volume5 and cortical thickness3 in auditory cortices; they also show differences in motor regions and in white matter organization of the spinothalamic tract6. The effects generally increase as a function of years of musical practice, again supporting an experience-dependent explanation. The cross-sectional design of such studies, however, cannot discern whether the anatomical effects are the cause or the consequence of the skill or knowledge that distinguishes the groups. Moreover, links to behavioral performance have not always been available, despite their importance to helping determine the relevance of structural effects to the presumed skill (Fig. 1 and Box 2).

Finally, it is not always clear whether training or ability should be associated with increases or decreases in relevant brain regions because of the complex relationship between anatomical changes and underlying functionality. A solution to these problems comes from longitudinal studies.(Figure 2)

Longitudinal imaging studies

One of the first such longitudinal MRI studies used voxel-based morphometry (see Box 1) to demonstrate increased gray matter density in the visual motion area bilaterally when people learn to juggle over a 3-month period7, and the same researchers later suggested that the changes are apparent after as little as 7 days of training8. Such experience-dependent macrostructural changes are not restricted to gray matter but can also be detected in white matter. Juggling training leads not only to increased gray matter concentration in occipito-parietal regions involved in visuo-motor coordination, reaching and grasping, but also to altered organization of underlying white matter pathways9 detected by fractional anisotropy (see Box 1). Similarly, practice of a complex whole-body balancing task results in increased gray matter in frontal and parietal cortex after just 2 days of training, and altered fractional anisotropy in corresponding white matter regions over 6 weeks of training10. However, the latter study found fractional anisotropy to change in the opposite direction, showing reductions over time with training. Although increases in fractional anisotropy are typically observed in association with maturation, development or learning, reduced fractional anisotropy might be observed if axon diameters increase or if a secondary fiber population matures in a region of fiber crossing (as was speculated to be the case here).

What aspect of learning experiences drives the observed brain changes? Both juggling and whole-body balancing are complex motor skills that involve procedural learning, but other studies provide evidence that even purely cognitive tasks, such as working memory training11, result in measurable changes in brain structure.

Experience-dependent versus pre-existing factors

Individual variation in anatomy affects perceptual and cognitive abilities (Box 2), but it is not known whether such correlations are related to differential environmental conditions or whether they reflect predispositions; that is, anatomical differences existing before the training or environmental event. The two options are not mutually exclusive, in that anatomical variation likely has many antecedents, including environmental, genetic and epigenetic ones.

Heritability studies in twin populations can quantify the degree to which environmental or genetic factors explain variation in gray or white matter measures. In gray matter, genetic influences are most notable in the frontal and temporal lobes, including areas related to language12. In white matter, genetic factors explain about 75–90% of the variation in fractional anisotropy in large regions, particularly in parietal and frontal lobes; other white matter regions, such as the corpus callosum, show much stronger evidence for environmental influence13.

Further evidence that not all the relationship between brain anatomy and individual differences in behavioral performance can be accounted for by environmental experience comes from studies where there is little opportunity for experience to have an effect. For example, when volunteers are taught to discriminate unfamiliar foreign speech sounds14, pre-existing variability in left auditory cortex structure, or in related white matter pathways, predicts the rate and/or outcome of learning. Similarly, although musical training probably influences auditory cortical anatomy, it does not entirely account for the relationship between auditory cortex volume and ability to learn pitch contours in a tone language15, or to discriminate melodies16. Together, these studies demonstrate that pre-existing anatomical features can affect learning rate and/or attainment, but they leave open the question of how anatomical changes induced by training may be influenced by the initial anatomical state of the relevant structure.

Underlying cellular and molecular mechanisms

The preceding sections demonstrated the power of human neuroimaging studies for detecting effects of specific training regimes on brain structure and relating these to complex behavioral changes. However, neuroimaging measures are difficult to relate unambiguously to underlying biology. Studies at the cellular and molecular level can identify candidate mechanisms to help explain neuroimaging observations.

Many approaches can be used to gain molecular and cellular evidence on experience-dependent microstructural changes, ranging from cell cultures to studies in behaving animals. Each experiment is typically only able to test for a limited set of structural changes, so building up a clear picture of how to understand systems-level effects requires integration across a wide literature. Observed changes can be broadly categorized into neuronal changes in gray matter, neuronal changes in white matter, and extra-neuronal change (Fig. 3). Neuronal changes in gray matter may include neurogenesis, synaptogenesis and changes in neuronal morphology. In white matter, changes in the number of axons, axon diameter, the packing density of fibers, axon branching, axon trajectories and myelination can be found. Extra-neuronal changes include increases in glial cell size and number, and angiogenesis. Fig. 3) Neuronal changes in gray matter may include neurogenesis, synaptogenesis and changes in neuronal morphology. In white matter, changes in the number of axons, axon diameter, the packing density of fibers, axon branching, axon trajectories and myelination can be found. Extra-neuronal changes include increases in glial cell size and number, and angiogenesis.

Any of these cellular changes may influence MRI signals (see Box 1). For example, variations in neuronal, glial and synaptic density may affect modalities sensitive to the proportion of cellular material versus extracellular space in a voxel, such as proton density imaging or relaxometry. Such features would therefore influence commonly used methods to assess gray matter change (voxel-based or tensor-based morphometry, cortical thickness) that rely on image intensity boundaries in T1-weighted images. Myelin will modulate measures sensitive to lipid content, such as relaxation times17 (and hence any method based on T1-weighted images), and measures that reflect the presence of barriers to water diffusion, such as fractional anisotropy18. Changes in the trajectory of white matter pathways could alter fractional anisotropy values in white matter and affect quantitative measures from modeling of complex diffusion profiles19. Angiogenesis could be detected by techniques such as contrast-enhanced imaging of blood volume or perfusion imaging of cerebral blood flow.

Ultimately, histological studies are required to make direct links between imaging measures and underlying mechanisms. For example, in one elegant study of gray matter plasticity, groups of mice were trained on different versions of a water maze, designed to depend on distinct brain systems, and volume measures were used to assess structural differences between groups20. As predicted, mice trained on a spatial version had growth in the hippocampus, whereas those trained on a cued version had growth in the striatum. The MRI-derived measures of growth correlated with GAP-43 (growth-associated protein-43) staining, a marker for axonal growth cones, and not with measures of neuronal size or number, suggesting that the MRI volume change reflected remodeling of neuronal processes, rather than neurogenesis.

Candidate mechanisms for gray matter changes

Most neuroimaging studies are motivated by hypotheses concerning neuronal structure or function. Yet non-neuronal components, such as vasculature and glial cells, will also influence MRI signals. Vasculature accounts for about 5% of gray matter21. In human gray matter, glia are believed to outnumber neurons by approximately 6 to 1, with varying ratios in different brain regions. In this section we will discuss evidence for both neuronal and non-neuronal activity-dependent changes in gray matter and will speculate on whether such changes may contribute to observed neuroimaging effects.

Neurogenesis

If a neuroimaging study detects increases in volume of a particular structure, then an attractive explanation is that there has been growth of new neurons. There is good evidence for adult neurogenesis occurring with learning in the hippocampus. Learning accelerates the maturation of the dendritic trees of new-born neurons and promotes their integration into functional hippocampal neural networks22. Transiently reducing the number of adult-born hippocampal neurons in mice impairs performance in memory tasks23, and conversely, increasing adult hippocampal neurogenesis by genetic manipulation improves pattern separation learning24.

What is the likelihood that neurogenesis underlies some of the observed neuroimaging changes with experience? Although adult neurogenesis produces thousands of new granule cells in the dentate gyrus every month25, this is a relatively small increase in total number of hippocampal neurons. Furthermore, although there have been reports of neurogenesis in the mammalian adult neocortex26, this is controversial. Thus, neurogenesis is likely a minor factor in MRI changes, particularly those found outside the hippocampus in association with learning. Animal studies using ferritin-based reporters27 and labeling precursor cells with iron oxide nanoparticles28 to visualize neuroblast migration with MRI may be helpful in answering this question.

Gliogenesis

Another explanation for MRI volume increases is increase in the number of non-neuronal cells. Unlike mature neurons, which cannot divide, astrocytes and oligodendrocyte progenitor cells (OPCs) retain the ability to divide in the adult brain. Indeed, it has been argued that all new cells in adult neocortex are non-neuronal; including glial cells and endothelial cells29. Gliogenesis, and structural plasticity of non-neuronal cells, occurs in response to learning and experience30 and might therefore be an important candidate mechanism for some of the MRI findings discussed above. The role of astrocytes in synaptic function, ion homeostasis, neuroenergetics and blood flow regulation in response to neuronal activity implicates these cells in changes detected by functional and structural MRI31.

In addition, microglia, the resident immune cells of the brain, have traditionally been considered only in the context of pathology, but new research is pointing to microglial involvement in structural and functional plasticity of synapses and dendrites during development and learning, and hence this involvement could have direct relevance for MRI-based measures. For example, in vivo microscopy shows that microglia have highly motile cell processes that continually survey the brain parenchyma and form transient contacts with synapses32. This process is experience-sensitive, as light deprivation reduces the motility of microglial processes, whereas reexposure to light reverses this response32 and is regulated by glutamate and ATP in an activity-dependent manner33.

Synaptogenesis and changes in neuronal morphology

Although we would argue that neurogenesis is unlikely to have a large role in MRI-detected experience-dependent change outside the hippocampus, other changes in neuronal morphology may nevertheless contribute. For example, motor skill learning is associated with synaptogenesis34 and changes in dendritic spine morphology35. One study of cerebellar changes in rats showed that whereas an increase in synapse number persists for 4 weeks, initial astrocytic growth (hypertrophy) declines in the absence of continued training, indicating differences in glial versus neuronal responses to experience36. Changes in dendritic spine structure can also persist after learning. For example, monitoring spine formation and elimination over time in the mouse cerebral cortex by in vivo microscopy has shown that the extent of spine remodeling correlates with behavioral improvement after learning37. A small fraction of new spines are preserved after learning, and these seem to provide a structural basis for long-term memory retention.

These distinctions in persistence of different types of structural change suggest that observing the time course of training-evoked change in neuroimaging studies may help to narrow down candidate mechanisms, but results thus far are mixed. Some studies on juggling, for example, have found that gray matter changes revert to baseline levels7, consistent with the time course of glial change observed in animal studies, but others have observed a persistence or even continued increases in these changes after the end of training9, 38, more consistent with synaptogenesis and spine formation.

Vascular changes

Training studies suggest that experience can alter the vasculature, particularly with regimes that increase physical activity. For example, experiments on middle-aged monkeys show that physical exercise increases histologically quantified vascular volume in the cerebral cortex in parallel with improved performance on cognitive tests; both effects are lost after a 3-month sedentary period39. Such vascular changes likely contribute to activity-dependent differences observed by structural MRI after training. One compelling study performed in both mice and humans showed that imaging measures of increased blood volume in the dentate gyrus of the hippocampus of exercising mice correlate with post-mortem measures of neurogenesis in this structure40. The authors argue that similar increases in blood volume observed using imaging in the hippocampus of exercising humans therefore likely also reflect neurogenesis, but this remains to be directly tested, and it is plausible that vascular changes could occur in some contexts even in the absence of neurogenesis.

Signaling pathways for gray matter changes

A broad range of activity-dependent signaling molecules and transcription factors are involved in regulating dendritic morphology and development of neurons and glia, most notably neurotransmitters, cytokines and growth factors. Summarizing the voluminous literature on signaling in neuronal plasticity is beyond the scope of this review. One example with supporting evidence from cellular to human imaging studies is brain-derived neurotrophic factor (BDNF) and its high-affinity receptor TrkB (tyrosine receptor kinase B), which have been widely implicated in neurogenesis and in morphological changes in dendrites during environmental experience and learning41. In human studies, polymorphisms in the BDNF gene are associated with variations in hippocampal volume42, memory performance43 and susceptibility to plasticity-inducing brain stimulation protocols44. BDNF can regulate development of oligodendrocyte progenitor cells and affect myelination45; however, activity-dependent regulation of myelination by BDNF has not been shown.

Far less attention has been given to activity-dependent regulation of glial development. Blocking neural impulse activity with tetrodotoxin reduces the number of astrocytes that develop in hippocampal cell cultures. This is explained in part by release of the neurotransmitter ATP from neurons, which in turn stimulates release of the cytokine leukemia-inhibitory factor from astrocytes46. Immune system signaling molecules affecting microglia, including the major histocompatibility complex (MHC)47 and C1q48, have been implicated in activity-dependent structural plasticity and remodeling of brain circuits.

Functional activity in neurons, astrocytes and blood vessels is tightly coupled and regulated by several signaling molecules. Among these, vascular endothelial growth factor (VEGF) has many activities affecting blood vessels, neurons, astrocytes, neurogenesis and cognition. Overexpressing VEGF or blocking endogenous VEGF in the hippocampus of adult mice affects neurogenesis, angiogenesis, long-term potentiation and memory49. However, the study in question found that the effects of VEGF manipulation on memory are evident before newly added neurons could have become functional, thus implicating effects of VEGF on mature neurons in the formation of memory.

Candidate mechanisms for white matter changes

Although it is clear that cellular changes in gray matter participate in learning, it is less obvious how structural changes in white matter might do so. However, any complex task requires transmission of information through a series of distant cortical regions with distinct task-relevant functions. Optimizing the speed or synchrony of impulse transmission could therefore be an important aspect of learning50. Changes in white matter, including axon diameter, the number of myelinated axons in a tract, the thickness of myelin, or other morphological features such as internodal distance determine the speed of impulse propagation and thus could contribute to increased functional performance with learning.

These structural properties of white matter influence neuroimaging measures. For example, diffusion imaging measures are sensitive to many tissue properties18, including variation in myelin51, axon diameter and packing density52, axon permeability18 and fiber geometry19.

Myelin

Many diffusion imaging studies of experience-dependent white matter plasticity propose change in myelin as a potential mechanism. This is a departure from the traditional view of myelin as passive electrical insulation, static and irrelevant to nervous system plasticity outside the context of injury or disease53. However, myelination is dynamic through development and into early adulthood, notably in the cerebral cortex, where the frontal lobes are the last regions to myelinate. Could activity-dependent modulation of myelin persist throughout adulthood?

Myelination of unmyelinated axons, or modification of the myelin sheath on myelinated axons, could participate together with synaptic remodeling in altering brain circuitry according to experience. OPCs remain resident in substantial numbers in the adult brain; indeed, one-third of OPCs in the adult mouse brain originate after adolescence54. These cells participate in repair after myelin damage, but they could in theory participate in learning if myelination of unmyelinated axons is stimulated by functional activity. Internodal lengths decrease in visual cortex of rhesus monkeys55 during normal aging, suggesting active remyelination throughout life.

Activity-dependent changes in myelin would provide a mechanism for experience-dependent regulation of impulse conduction velocities. Physical activity is known to affect conduction velocity, as conditions of inactivity, such as during bed rest or outer space missions, temporarily reduce conduction velocities56. Increasing motor activity in rats is associated with altered myelin thickness and axon diameter in peripheral nerves57. The results suggest that activity not only influences the formation of myelin but also influences the maintenance and morphology of the sheath after myelination is complete.

Several neuroimaging studies have reported changes in white matter structure with learning in adults9, 10, 11, yet sensitivity of myelination to environmental experience seems to be reduced in adulthood. Although the volume of the splenium of the corpus callosum increases by 10% in adult rats exposed to an enriched environment, histological analysis has shown that this is caused by an increase in number of astrocytic cell processes and branching of unmyelinated axons, rather than an increase in myelin58.

Combined histological and MRI studies on animals are required to answer the question of whether myelin changes underlie the white matter plasticity observed with imaging. A recent study of rats trained in the Morris water maze showed changes in diffusivity or anisotropy in several brain regions, including cingulate, piriform and somatosensory cortex, dentate gyrus and corpus callosum59. Similar effects were detected, albeit with lower magnitude, in older rats. Histological analysis confirmed that gray matter regions with decreased diffusivity also show an increase in astrocyte cell volume, whereas the increased fractional anisotropy observed in corpus callosum is associated with increased staining for myelin basic protein.

Activity-dependent axonal sprouting, pruning or re-routing

In hippocampus, sprouting of mossy fiber axons has been observed after induction of long-term potentiation60 and after spatial learning61, but similar changes are induced by forced and voluntary physical exercise in the absence of learning62. Pruning of axons is guided by activity-dependent competition to refine functional circuits. Using a mouse genetic system in which restricted populations of neurons in the hippocampus can be inactivated, Yasuda et al. showed that a similar activity-dependent competition participates in establishment of functional memory circuits63. That study reports that inactive axons in the hippocampus are eliminated by activity-dependent competition with active axons, and in the dentate gyrus, which undergoes neurogenesis throughout life, axon refinement is achieved by competition between mature and young neurons.

There is some evidence for changes in long-range cortico-cortical connectivity occurring with learning and with recovery from damage64. For example, when macaque monkeys learn to use a rake to retrieve food pellets, cells in the parietal cortex, where new bimodal responses are found, also show a new pattern of anatomical connectivity: inputs from certain visual areas were detected in trained animals but not in untrained animals, suggesting the possibility of a rebranching of fibers in response to training, to allow particular types of visual information to reach parietal regions. Similar rewiring has been observed in response to damage in a squirrel monkey model65. Such changes in the route of fiber bundles should affect imaging measures reflecting the directional preferences of water diffusion. For example, diffusion MRI models of complex fiber structure19 could be used to detect subtle changes in tract geometry.

Signaling pathways for white matter changes

Recent in vitro studies are beginning to elucidate the molecular signals and neurotransmitter release mechanisms that could allow activity in an axon to influence myelinating glia and white matter microstructure. Synapses do form transiently on some OPCs in white matter66, 67, but their function is unknown. Recently a nonsynaptic mechanism of neurotransmitter (ATP) release from axons has been described taking place through volume-regulated anion channels in axons that become activated by trains of action potentials68. Activity-dependent release of ATP from axons has been shown to regulate myelination in the peripheral69 and central nervous systems70, 71. The diverse range of membrane receptors expressed in oligodendrocytes suggest that other types of cell-cell communication molecules72, 73, 74, including diffusible and cell surface molecules, could influence OPC proliferation, migration, differentiation, survival and myelin formation, in an activity-dependent manner.

In addition to effects on OPC development, new evidence shows that electrical activity in axons can control the complex sequence of cellular events necessary for myelination. Immature oligodendrocytes populate the human cerebral white matter throughout the later half of gestation, yet most do not commit to myelinogenesis until 3 months later75, demonstrating a dissociation between events that regulate maturation of oligodendrocytes and their commitment to myelinogenesis. Myelin formation requires cell recognition to myelinate the appropriate axon, the formation of adhesive contacts, elaboration of vast areas of cell membrane to form myelin sheets, wrapping many layers of membrane around axons, and the removal of cytoplasm from between the wraps of myelin to form compact stacks of lipid membrane, all of which might be influenced by signaling from electrical activity in axons. Impulse activity regulates expression of an adhesion molecule on neurons, L1-CAM (L1 cell adhesion molecule), that is essential for myelination76, and recently vesicular release of the neurotransmitter glutamate along axons has been shown to stimulate the initial events in myelination. Both the cholesterol-rich signaling domains between axons and oligodendrocytes and the local synthesis of myelin basic protein from mRNA in the oligodendrocyte process are stimulated by the activity-dependent release of glutamate from axons77. This would preferentially myelinate axons that are electrically active and increase the speed of conduction through these functionally active circuits. This process could therefore underlie some of the changes in white matter seen in MRI studies.

Interrelations between neuron and glial changes

Considering activity-dependent changes in neurons and glia independently is highly artificial, as the two cell types are tightly coupled in both gray and white matter tissue through many interactions and pathways of communication. Myelination is regulated by axon diameter, for example. Thus, changes in axon diameter during learning could in turn cause oligodendrocytes to alter the thickness of the myelin sheath. Conversely, myelinating glia can regulate axon diameter and even the survival of axons73. Axons that become demyelinated can degenerate, and this can lead to the death of neurons78. Regardless of which cell initiates the response, both axons and glia may be affected by impulse activity (directly or indirectly) through their close association.

An example of this intimate relationship is provided by the protein Nogo-A. Nogo-A is a myelin protein that interacts with the Nogo-66 receptor 1 (NgR1) in axons to inhibit growth cone motility and axon sprouting. Several other myelin proteins, including MAG (myelin-associated glycoprotein) and OMgp (oligodendrocyte myelin glycoprotein), interact with the Nogo receptor, making myelin a potent inhibitor of axon sprouting, fasciculation, branching and axon extension79, as well as affecting synapse formation, synapse morphology and activity-dependent synaptic strength80. The function of myelin proteins in suppressing axon sprouting is thought to limit structural plasticity of neural circuits after refinement through environmental experience and thus to preserve the refinements. Myelin is therefore important in determining the critical period for learning, and it is central to activity-dependent development of neural circuits.

More recently, it has been determined that Nogo-A is also expressed in some neurons. Ablation of this gene in neurons leads to longer neurites, increased fasciculation and decreased branching of cultured dorsal root ganglion neurons, and anti-Nogo-A antibodies lead to aberrant innervation of the hind limbs of chick embryos79. In Nogo-A we see a molecule coupling neurons and glia, white matter and gray matter, to structural modifications of brain circuits that likely underlie changes seen with MRI during learning. Nogo-A may be exceptional in this respect, or simply the first of many molecules yet to be recognized controlling activity-dependent interactions between neurons and glia in gray and white matter.

Concluding remarks

Human imaging studies identifying experience-dependent structural changes in brain gray and white matter have rightly generated much excitement in recent years. A future challenge is to determine the cellular changes that underlie these macrostructural observations. Meeting this challenge requires greater cross-talk between those studying human populations and those working with animal models, and greater integration of techniques. Animal studies in which both imaging and histological measures can be taken in parallel, in particular, will help to establish the relative contributions of different cellular processes to the MRI effects, keeping in mind that multiple, coordinated cellular responses may be associated with a single MRI-based variable.

In future, greater use of multimodal imaging approaches in humans should provide increased specificity to better discriminate specific types of cellular changes during learning and in relation to behavior. The MRI technique of magnetization transfer provides a good example of the potential for complementarity across modalities because it is thought to be differentially sensitive to myelination. In magnetization transfer, the magnetization of macromolecules, such as those contained in myelin, is selectively altered (saturated) so that its effect can be detected through exchange with observable liquid spins. Magnetization transfer has already been used to examine natural variation of white matter composition in healthy populations81 and therefore has distinct potential to be used as a more specific probe of neural plasticity associated with learning. Similarly, myelin measures can be derived from maps of multi-exponential T2 relaxation times82 and vital stains for myelin sheaths can be imaged with positron emission tomography83. These myelin-specific measures could complement measures derived from MRI techniques such as diffusion tensor imaging or voxel-based morphometry that are sensitive to several features of tissue organization and microstructure.

Pushing the boundaries of image acquisition with sophisticated hardware can provide a new window on tissue microstructure at a level not previously achievable in human studies. In gray matter, for example, imaging at ultra-high resolution, and with multiple signal modalities, allows measures to be taken in specific cortical layers84 or hippocampal subfields85. New developments in modeling of complex tissue architecture can provide greater sensitivity to specific cellular features. In white matter, for example, diffusion imaging can be adapted to generate axon diameter distributions86 or estimates of myelin microstructure87. Such advances offer great potential to further our understanding of brain structural variation with learning and behavior. Despite the many obstacles that will have to be overcome, human neuroimaging and cellular and molecular neuroscience have much to gain from further interactions in both directions. "!

Täällä on muuten artikkeli, jossa spekuloidaan ajatuksella, että emotionaalinen signalisaatio olisi nimenomaan astrosyyttigliasolujen välistä (se voi levitä silmänräpäyksessä miljooniin yhteyksiin ja leimata kaiken jollakin "värillä" mitä aivoissa tietyllä hetkellä tapahtuu), ja esitetään myös, että tahtokin toimisi juuri noilla "kaapeleilla". Astrosyyttien kautta kulkeva signalisaatio ei näy magneettikuvissa, mikä selittäisi (pois) mukamas "aivopäätökset sekunteja ennen tietoisia päätöksiä": Päätös ei ole näkynyt kuvissa, vaan pelkästään sen valmistelu. Muutoin tämä artikkeli ei ole erityisen hyvä, siellä mm. siteerataan Kyseenalaista Antonio Damasiota. Täällä on sitten niitä "sellaisia" "tutkimuksia", joissa on tuossa huijattu tai ainakin menty muuten vaan metsään:

https://link.springer.com/article/10.1007%2Fs10827...

www.nature.com/neuro/journal/v11/n5/full/nn.2112.html

www.rifters.com/real/articles/NatureNeuroScience_S...

homepages.abdn.ac.uk/a.hunt/pages/dept/L4Option/Haggard2005.pdf

web.gc.cuny.edu/cogsci/private/wegner-trick.pdf

Keskustelua:

http://www.tiede.fi/keskustelut/psykologia-aivot-j...

Seurannaista hölynpölyä:

http://www.talentumshop.fi/talecom/tuoteinfo/978-9...

Risto Koivula

Brasilian kahden suurimman yliopiston, valtiollisen ja yksityisen, asianomaiset laitokset ovat asettuneet selkeästi ja näkyvästi Fieldsin teorian kannalle "eurotiedettä" vastaan:

https://hameemmias.vuodatus.net/lue/2015/10/paatok...

" Tahtotoiminnot pelaavat astrosyytti-gliasolujen ohjaamilla nopeilla synaptisilla psosesseilla (kuten myös mm. psyykkinen kuvanmuodostus havainnossa) eikä se näy magneettikuvissa jo siitäkään syystä, että astrosyyttien magneettikenttä on tasainen eikä vaihtuva kuten neuroneilla.

https://www.sciencedirect.com/science/article/pii/...

Astrocytes and human cognition[/url]: Modeling information integration and modulation of neuronal activity

Alfredo Pereira Jr a), Fabio Augusto Furlan b)

http://www.google.fi/url?q=http://jcer.com/index.p...

http://www.msmonographs.org/article.asp?issn=0973-...

a) Institute of Biosciences, State University of Sao Paulo (UNESP), Campus Rubia Jr., 18618-000, Botucatu-SP, Brazil

b) School of Medicine, University of Marília[/url] (UNIMAR), Marília-SP, Brazil "

http://translate.google.com.br/translate?js=n&prev=_t&hl=pt-BR&ie=UTF-8&layout=2&eotf=1&sl=pt&tl=en&u=http://www.rc.unesp.br/[url=http://nasc.in/southamerica/index.php?option=com_content&view=article&id=87:university-of-marilia-unimar-faculty-of-medicine-&catid=9:brazil

(Tässä on takana Brasilian Valtionyliopisto ja suurin ei-valtiollinen yliopisto, ja sanoma on, että Fieldsin mukaan edetään:

url=http://network.nature.com/groups/bpcc/forum/topics/6747?page=1

Pereira: " I have read most of the popular text on brain function written by Nobel Laureates, prominent neuroscientist, philosophers, linguist and “science writers”. None can match “The Other Brain” as far as thoroughness of scientific facts and ease or reading. It is a real “page turner”. It is the only book on brain function that I could not put down until completed. Until you read this remarkable book about glia, “the other half of the brain”,your knowledge of brain function is far from complete.")

" Recent research focusing on the participation of astrocytes in glutamatergic tri-partite synapses has revealed mechanisms that support cognitive functions common to human and other mammalian species,such as learning,perception,conscious integration, memory formation/retrieval and the control of voluntary behavior. Astrocytes can modulate neuronal activity by means of release of glutamate, D-serine, adenosine triphosphate and other signaling molecules, contributing to sustain, reinforce or depress pre- and post-synaptic membranes. We review molecular mechanisms present in tripartite synapses and model the cognitive role of astrocytes. Single protoplasmic astrocytes operate as a ‘‘Local Calcium waves Hub’’, integrating information patterns from neuronal and glial populations. Two mechanisms, here modeled as the ‘‘domino’’ and ‘‘carousel’’ effects, contribute to the formation of intercellular calcium waves. As waves propagate through gap junctions and reach other types of astrocytes (interlaminar, polarized, fibrous and varicose projection), the active astroglial network functions as a ‘‘Master Hub’’ that integrates results of distributed processing from several brain areas and supports conscious states.

Response of this network would define the effect exerted on neuronal plasticity (membrane potentiation or depression), behavior and psychosomatic processes. Theoretical results of our modeling can contribute to the development of new experimental research programs to test cognitive functions of astrocytes.

1. Introduction

Although astrocytes compose at least one half of human brain tissue volume, until two decades ago mostly passive functions were attributed to these glial cells, such as giving structural, metabolic and functional support for neurons. However, a growing number of ‘in vitro’ and ‘in vivo’ results support the conception that unipolar cells reside in the deep layers of the cortex, near the white matter (and) extend one or two long (up to 1 mm in length) GFAP-positive processes away from the white matter’’ (Oberheim et al., and Araque, 2005; Haydon and Carmignoto, 2006; Wang et al., 2006b; Fellin et al., 2006; Genoud et al., 2006; Winship et al., 2007; Schummers et al., 2008; Halassa et al., 2009). In an evolutionary approach, Banaclocha states that ‘‘in the leech, the astrocyte–neuron ratio is 1:25; in Caenorhabditis elegans 1:6; in rats and mice 1:3. In humans, the astrocyte-to-neuron ratio is approximately 3:2. This exponential increase of astrocytes cannot be explained solely on increased glial metabolic support. Alternatively, it is plausible that increasing numbers and organization of astrocytes implicates a role for these cells in the evolution of increasingly complex brain functions’’ (Banaclocha, 2007). Evidence for this role is an increase in glia-to-neuron ratio in human dorsolateral frontal cortex.

Direct applications of these results for an understanding of human cognition and emotion are beginning to emerge in the fields of neurology and psychiatry. Astrocytes are involved in the etiology of several neurological disorders as epileptic seizures (Willoughby et al., 2003; Silchenko and Tass, 2008; Reyes and 2009; Kuchibhotla et al., 2009), abusive ethanol consumption (Gonzalez and Salido, 2009) and other drugs (Haydon et al., 2009), schizophrenia (Halassa et al., 2007a; Mitterauer, 2009), depression (McNally et al., 2008) and mood disorders (Lee et al., 2007), among other dysfunctions (Antanitus, 1998; De Keyser et al., 2008). A recent hypothesis about the origin of psychiatric disorders focus on blood–brain barrier (BBB) breakdown and brain astrocyte dysfunction leading to disturbed cognition, mood, and behavior: These events ‘‘are initiated by a focal BBB breakdown, and are associated with dysfunction of brain astrocytes, a local inflammatory response, pathological synaptic plasticity, and increased network connectivity’’ (Shalev et al.,2009).

Other kinds of glial cells – reviewed by R. Douglas Fields (2009) – have also been shown to be relevant for health and disease, as oligodendrocytes in schizophrenia and microglia in degenerative disorders.

( url=http://nakokulma.net/index.php?topic=10081.0 )

In this emerging paradigm, glial cells are envisaged as the main target for new psychiatric drugs. According to Halassa et al. (2009), ‘‘These discoveries begin to paint a new picture of brain function in which slow-signaling glia modulate fast synaptic transmission and neuronal firing to impact behavioral output. Because these cells have privileged access to synapses, they may be valuable targets for the development of novel therapies for many neurological and psychiatric conditions’’."

(Tämä artikkeli on ilmestynyt ennen Fieldsin kirjaa. Kirjassaan Fields käsittelee myös astrosyyttien suorittamaa synapsien ohjausta: "Thisis exactly what astrocytes do at a synapse!"

http://books.google.fi/books?id=2nmHpXPmV80C&pg=PA...)

" 11. Astrocytic network mediates voluntary behavior

The diagram (Fig. 10) provides an overview of cognitive functions of astrocytes in brain function. The Master Hub is activated by means of signaling from neurons to astrocytes in tripartite synapses, as well as panglial communication triggered by signaling molecules carried by blood (e.g. hypothalamic function; see Gordon et al., 2009; Panatier, 2009) and cerebrospinal fluid.

The above diagram is a simplified view of interactions of main functional systems in the human brain. Neuronal and astroglial networks are represented separately. The ‘‘Executive System’’ includes, besides association cortices, also the hippocampal-entorhinal neuronal system.‘‘Emotional neurons’’ are mostly in the limbic system, but the term applies to all neurons that process information related to emotional phenomena. It should be clarified that, according to the presented model, such neurons detect (e.g. amygdala neurons) and process (e.g. orbitofrontal neurons) emotional information, but do not convey the feeling (e.g., pain, hunger) elicited by the emotional state (e.g., tissue injury, empty stomach). Feeling is proposed to be a function of the astrocytic network. Each feeling is generated by the response of astrocytes connected to the neurons that detect and process the respective information patterns.

Voluntary responses require the participation of executive neurons that make all logical operations necessary to implement coherent behavior. Astrocytes only ‘‘approve’’ or ‘‘veto’’ executive plans. An important feature of the diagram is that astrocytes cannot directly depress basic emotional neurons (e.g. there is no habituation to pain), but can indirectly contribute to their inhibition by means of executive mediation (e.g., repressing an automatic aggressive response). Psychosomatic effects are mediated by the actions of efferent neurons (e.g., on the endocrine and immune systems) by means of diffuse blood and cerebrospinal fluid signaling. They require conscious processing of the stimulus, but the generation of the effect is unconscious.

We exemplify the explanatory power of the diagram with the example of Conditioned Taste Aversion (CTA). This is a kind of learning process present in several mammalian species, consisting of an acquired aversion for previously ingested food that caused digestive pain and/or damage. Although the learning process is mostly unconscious (leading to the formation of non-declarative memory), there are three phases in the whole process that imply conscious processing:

(a) Initial tasting of the food. Although the aversion is not generated by the food having a bad taste, this tasting is necessary to create a register of what it tastes like;

(b) Unpleasant (conscious) sensation of nausea and/or digestive pain caused by the food;

(c) Tasting and recognition of the food after conditioning, both necessary to trigger the aversion behavior.

The CTA process begins with the sensing of food properties.Perception of properties of the stimulus (e.g., how it tastes) ismediated by thalamic relay neurons that transmit the signal to somatosensory cortex neurons (Perceptual Cortical Neurons in the diagram). These neurons interact with higher level neurons and neighboring astrocytes, generating a taste and other sensations elicited by the stimulus. When the taste (itself not relevant for CTA and digesting experience (relevant for CTA) are satisfactory, astrocytes reinforce neuronal synapses involved in the processing of the stimulus by means of membrane potentiation (green arrows). The signal is also transmitted to subcortical neurons belonging to circuits that control feelings of hunger and satiation (Basic Emotional Neurons). Interaction with the basic emotional system can trigger an automatic behavior (activation of Motor Neurons) of swallowing or rejecting the food.

When, after ingestion, a nausea or digestive pain occurs, astrocytes induce the in-hibition of basic emotional neurons that mediate the response,by means of potentia- ting the respective inhibitory neurons of the Executive System, thus conditioning the response to new presentations of the same kind of stimulation. In this case, there will be both automatic and voluntary responses to the stimulus. The automatic response, mediated by an interaction of subcortical relay neurons with the basic emotional system, consists of avoidance. The voluntary response, following the sensing of the taste, can be e.g. a throw off.

12. Concluding remarks

In this review of recent astrocyte research and related psychophysiological modeling we made a set of theoretical claims which – if true – would correspond to a scientific revolution in brain sciences, moving from a neurocentric to an astro-centric perspective on cognitive and emotional processing. In spite of the boldness of the claims, they are all experimentally tangible and lead to exciting new perspectives in the interdisciplinary field of Physiological Psychology. Our model favors the development of new experimental research programs to test the cognitive function of astrocytes, by means of the development of new methods and techniques, or by reinterpreting results obtained with classical tools as the several modalities of EEG.

Among the future experimental possibilities opened by this approach, we would like to highlight the following. An exciting prospect would be testing the proposed association of different kinds of human astrocytes identified by Oberheim et al. (2006, 2009) with the cognitive functions we attribute to them (operating as Local or Master Hubs). Another important line of investigation is paying (more) attention to behavioral effects of genetic and pharmacological knockout of astroglial proteins to evaluate cognitive functions, e.g. by means of the usage of paradigms for voluntary and automatic responses. Also the observation of behavior of pannexin knockout mice may lead to important discoveries, since this protein is involved in ATP mechanisms relevant for the propagation of calcium waves. In contrast, analysis of behavioral effects of drugs – like fluorcitrate – that have effects on single astrocytes cannot confirm or disconfirm the astrocentric hypothesis, since the crucial cognitive effect may be on the neurons that interact with the astrocytes. If the hypothesis happens to be true, then the final target of action of all general anesthetics has to be the astrocytic network.

From this reasoning, several testable hypothesis can be raised and experimentally proven, e.g.that the anesthetic effect of halothane is on astroglial – not neuronal – gap junctions, or that the anesthetic action of ketamine and other NMDAR blockers impair the operation of the Master Hub. Other important predictions are that the Master Hub is functionally deactivated during dreamless SWS and severely disturbed during generalized epileptic seizures with loss of consciousness.

The development of new ‘in vivo’ imaging technologies, which has already begun with two-photon microscopy combined with fluorescent markers, may bring new and important evidence about the cognitive role of astrocytes. We have suggested (Pereira, 2007) the development of ultraviolet laser technology for imaging of large-scale calcium ion population movements in the brain. More conventional techniques may also be reinterpreted in this new perspective. Astrocyte activity may contribute to scalp and intercellular EEG registers, as well as to conscious modulation of brain rhythms in neurofeedback therapy (for an overview of the sources of EEG signals, see Buszaki, 2006).

Astrocytes may also become the main target of electric and magnetic therapeutic methods. According to Banaclocha, ‘‘it has been well established that astrocytes produce steady state (DC) magnetic field while neurons produce time-varying (AC) magnetic fields’’ (2007). In this case, astrocytes are not directly involved in the effects of electroshock (using AC), but there is a possibility of therapeutic use of astrocyte stimulation by means of DC. It has also been suggested that deep-brain stimulation, which in many cases relieves the symptoms of Parkinson’s disease, may act on astrocytic calcium waves that coordinate the activity of large populations of neurons controlling movement (Douglas Fields, 2009).

Last but not the least, we would like to stress the importance of having a theoretical model of astrocyte cognitive functions, even if it is still sketchy and incomplete, to inspire new research programs.

In the spirit of modern science, we will feel content if any (or all) of our assumptions and claims are corrected by future experimental results, leading to progress of knowledge about how animals execute cognitive operations."

"Eurotiede" tulee saamaan vastaavanlaiset kilpailijat kuin englantilaisella ja por-tugalilaisella, myös espnjalaisella ja ranskalaisella kieli- ja klutturialueella. Noiden alueiden sisällä on aina käyty kilpailua tieteelisestä auktoriteetista, ja muustakin menetyksestä, ja myös henkilöistä...

Risto Koivula

http://en.cnki.com.cn/Article_en/CJFDTotal-XLKX201...

Are Mirror Neurons the “Holy Grail” of Cognitive Science?

Chen Wei; Wang Yin;

Department of Psychology, Shaoxing University; Center for Language and Cognition Research, Zhejiang University;

School of Psychology, New York University;

The discovery of mirror neurons in the 1990s has led to excitement in the cognitive neuroscience. Mirror neurons have received a great deal of attention from specialists both in the scientific field and public media. More and more abilities have been attributed to these neurons; they are even hailed for what they "do for psychology as DNA did for biology". And a series of related studies have given rise to "a revolution in understanding social behaviors". Mirror neurons have been implicated in a wide variety of functions, such as action-understanding, imitation, empathy, theory of mind, language evolution, telepathy, self-awareness, substance use disorders.

Mirror neurons are viewed as the "holy grail" of cognitive science. The assumption that mirror neurons play a key role in social cognition is not without controversy, however. This review shows that the current data about mirror neurons are very mixed and that those studies that use weakly localized measures to examine the functions of the mirror neuron(system) are hard to interpret.

Firstly, some theorists misuse and abuse the operational definition of mirror neurons. Mirror neurons are a class of visuomotor neurons activated by both the execution and the passive observation of object-related actions. Cells having this property were only found in macaques within the premotor cortex (area F5), and in the rostral part of the inferior parietal cortex (PF).

Secondly, the idea that mirror neurons exist in human beings remains controversial, although the human homolog of the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) can be seen as a classic human mirror neuron system.

We systematically review the empirical foundations of the mirror neuron research; it turns out that unless one can manage to evade all the ethical, technical, and procedural limitations imposed on human brain research, no complementary research can be carried out to demonstrate the existence of mirror neurons in the human brain convincingly with microelectrodes or any other technique operations at the neuronal level.

Last but not the least, claiming the mirror mechanism plays a crucial role in understanding the behaviors of others does not imply that there are no other mechanisms involved in action understanding. Some of these mechanisms based on the social brain are basic and cannot be ignored, relying on the association between a given stimulus and its corresponding effect.

The mirror neuron(system) and its mirror mechanisms cannot be used to account for empathy, imitation and mindreading or explain other social cognition phenomena.

It is an outdated ideology as a modularity of mind. The future study for mirror neurons must attempt to answer the following questions.

(1) How can an agent make a distinction between the intention of self-action and those of others? And how can someone's mirror neuron(system) and other social brains cooperate in this processing?

(2) How can an agent make an understanding outcome prediction of an action? It depends not only on the action itself, but also on the context in which the action is embedded. "

Risto Koivula

https://www.ncbi.nlm.nih.gov/pubmed/18479959

" Trends Cogn Sci. 2008 Jun;12(6):225-9. doi: 10.1016/j.tics.2008.03.005. Epub 2008 May 12.
Unbroken mirrors: challenging a theory of Autism.
Southgate V1, Hamilton AF.
Author information
Abstract

The 'broken mirror' theory of autism has received considerable attention far beyond the scientific community. This theory proposes that the varied social-cognitive difficulties characteristic of autism could be explained by dysfunction of the mirror neuron system, thought to play a role in imitation. We examine this theory and argue that explaining typical imitation behavior, and the failure to imitate in autism, requires much more than the mirror neuron system. Furthermore, evidence for the role of the mirror neuron system in autism is weak. We suggest the broken mirror theory of autism is premature and that better cognitive models of social behavior within and beyond the mirror neuron system are required to understand the causes of poor social interaction in autism.

PMID:
18479959
DOI:
10.1016/j.tics.2008.03.005

[Indexed for MEDLINE]

https://www.cell.com/trends/cognitive-sciences/fulltext/S1364-6613(08)00114-9

https://www.cell.com/trends/cognitive-sciences/pdf/S1364-6613(08)00114-9.pdf

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