Tämä  puoskaritiede on lähtenyt liikkeelle jo aikanakin 12 vuotta aikai-semmin Britanniasta NATO-tieteen Euroopan-keskuksesta (hyvässä ja pahassa, olen itsekin käynyt luennoimassa ja julkistamassa tutkimustu-loksiani siellä, motkaissut olan takaa oman alan "eurotiedettä", ettei sen puoleen...), jo 8 vuotta ennen Giacomo Rizzolattin ilmeisiä väären-nöshavaintoja (2) samalla, alun perin Ragnar Granitin kehittämällä elektrodimenetelmällä, saman porukan ja lisäksi tamperelaisen Jari K. Hietasen toimesta, tästä tarkemmin lopussa. (1)


Imitation, mirror neurons and autism

Article · Literature Review (PDF Available) inNeuroscience & Biobehavioral Reviews 25(4) · July 2001with317 ReadsDOI: 10.1016/S0149-7634(01)00014-8 · Source: OAI

https://www.researchgate.net/publication/28763620_Imitation_mirror_neurons_and_autism


Justin H G Williams

Department


Thomas Suddendorf

Thomas Suddendorf


Andrew Whiten

ImportedProfilePhoto.jpg

Andrew Whiten

David I Perrett47.07

Perrettmedium.jpg

David I. Perrett

(Häijyn näköistä porukkaa...)


Abstract

Various deficits in the cognitive functioning of people with autism have been docu-mented in recent years but these provide only partial explanations for the condition. We focus instead on an imitative disturbance involving difficulties both in copying actions and in inhibiting more stereotyped mimicking,such as echolalia. A candidate for the neural basis of this disturbance may be found in a recently discovered class of neurons in frontal cortex, 'mirror neurons' (MNs). These neurons show activity in relation both to specific actions performed by self and matching actions performed by others, providing a potential bridge between minds. MN systems exist in primates without imitative and ‘theory of mind’ abilities and we suggest that in order for them to have become utilized to perform social cognitive functions, sophisticated cortical neuronal systems have evolved in which MNs function as key elements. Early developmental failures of MN systems are likely to result in a consequent cascade of developmental impairments characterised by the clinical syndrome of autism.


(PDF) Imitation, mirror neurons and autism.

Available from:

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Contents
1. Introduction: the basis of autism ...........................................................287
2. The role of early imitation ......................................................................288
3. Imitation in autism ....................................................................... ...........289
4. Neurobiology of imitation .................................................................. ....289
5. The functional signi®cance of mirror neurons ....................................290
5.1. Speech ............................................................................ ......................290
5.2. Theory of mind ..................................................................... ............. ..290
5.3. More basic intersubjective phenomena: emotional contagion and shared attention........................................................................................................ 290
5.4. Imitation ..................................................................................................291
6. Mirror neurons and autism .................................................................... 291
7. Autism, executive functions and mirror neurons .................................291
8. Neuroimaging mirror neurons and `theory of mind' ............................292
9. Testing the hypothesis ........................................................................... 292
10. Conclusion ............................................................................................. 293
References ...............................................................................................---- 293


(PDF) Imitation, mirror neurons and autism. Available from:

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1. Introduction: the basis of autism

The autistic spectrum disorders are increasingly being recognised as an important cause of social disability [1]´and have been the focus of a ¯urry of research in the last decade [2±5].Here,we suggest that juxtaposing some of these psychological findings with recent discoveries in neurobiology offers the prospect of a new and potentially powerful model of both early social functioning and the disorders in it that are associated with autism.

The autistic spectrum disorders are characterised by impairments in social interaction, imaginative ability and not specific to the condition such as global developmental delay, aggression or sleep disturbance.

2. The role of early imitation

The possibility that deficits in imitation might be particularly intimately connected with the earliest developmental stages of autism was first set out systematically by Rogers and Pennington [21]. According to these authors, imitation might fill at least two of the three gaps left by the ToM explanation noted above: first, imitation has characteristics suggesting that the mechanisms underlying it could be precur- sors (perhaps the first that can be identified in infancy) to full ToM; and second, imitation may also be funda-mental to the other, broader kinds of social deficits seen in autism. The relationship between imitation and the third group of (largely non-social) deficits listed above is one we shall discuss once other parts of our model have been explained.

Rogers and Pennington [21] collated existing empirical evidence of imitation deficits in autism, which we discuss in the following section. First, however,some key theore- tical bases for a link between imitation mechanisms and later developing ToM need to be recognised.

Imitation and the attribution of mental states bear some fundamental resemblances [22, 23]. Both involve translating from the perspective of another individual to oneself. Thus in accurately reading the belief of another, one essentially copies the belief into one's own brain, creating a `second-order' representation of the other's primary repre-sentation of the world (and, of course, not confusing it with one's own beliefs, at least in the normal case). Conversely, in imitating, one must convert an action plan origina-ting from the other's perspective into one's own. A more specific linkage between imi-tation and ToM is implied by the fact that one of the two principal models of how ToM operates is designated the `simulation' theory [24].Its rival is the `theory theory', which sees the child acting somewhat like a young scientist,observing patterns of beha-viour in others, and developing theories about mental states to explain and predict them. The simulation theory instead proposes that children come to read minds by `putting themselves in the other's shoes', and using their own minds to simulate the mental processes that are likely to be operating in the other.

`Acting as if you are the other's simulation is thus at the covert, mental level akin to what is involved at the overt level in imitation. Current views include the possibility that both `simulation theory' and `theory-theory' processes are at work in the human case [25].

Meltzoff and Gopnik [26] reviewed evidence for imitation in the earliest phase of in-fancy and proposed that this could provide a key starting-state for the development of ToM. The nub of their hypothesis is that the new-born's capacity to translate between the seen behaviour of others and what it is like to perform that same behaviour offers a crucial basis for recognising the linkage between mental states and actions.

There are, thus,substantial theoretical reasons for considering imitation as a prime candidate for the building of a ToM. Rogers and Pennington's theory [21] was that at the root of autism is `impaired formation/co-ordination of specific self-other represen-tations', manifest first in impaired imitation,followed by a cascade of impairments in emotion-sharing, joint attention and pretend play (thus including the broad range of socialde®cits), and ToM. What, then, is the evidence for imitation being affected in autism?

3. Imitation in autism

Evidence for an imitative deficit in autism has been reviewed elsewhere [21, 27 ± 29]. None of these reviews is comprehensive, but together they cite 21 experimental studies of the imitative competence of individuals with autism. The studies have been heterogeneous with respect to the mental ages tested, the types of control groups used and the imitation tests themselves, but only two studies did not find an imitative deficit in the autistic samples and then possibly because of the simplicity of the tasks ,leading to ceiling effects. Smith and Bryson [27] conclude that the literature shows a `consistent fnding that people with autism do not readily imitate the actions of others'. Furthermore it is worth noting the magnitude of the imitative deficit. For instance, Ro-gers et al. [30] detected group differences of approximately 1.5 standard deviations between the autistic and control group means. More recently, Hobson and Lee [31] found that only 1 out of 16 (6%) subjects imitated the style of one of their tasks, com-pared to 12 out of 16 (75%) controls. A number of studies have detected significant group differences with just 10 subjects per group. The magnitude of this deficit then can be at least as great if not greater than the `theory of mind' deficit. Rogers [28] additionally notes the difficulties faced by carers in intensively teaching imitation to young children with autism.

Deficits in the imitation of `symbolic' elements (such as pantomiming brushing one's teeth with a non-existent toothbrush) might be expected in view of the diagnostic cri-teria;thus of special interest are those concerning basic body movements or gestures. These were first demonstrated by DeMeyer et al. [32] and have since been replicated in at least nine further studies [27±29].

Rogers [28] concludes that `every methodologically rigorous study so far published has found an autism-specific de®cit in motor imitation'. The conclusion that the imita-tive deficit may be operating at such a fundamental level is important to our synthesis with neurobiological findings discussed further below.

The reason for difficulties in imitation associated with autism remains unclear but some clues may come from an examination of the type of imitative deficit present.

Firstly, imitation of meaningless gestures would appear to be affected more than imitations of actions with objects [30].

Perhaps the use of objects in some tests may offer a `prop', helping to shape a mat-ching response; by contrast, difficulties in copying raw gestures underlines the more basic nature of the imitative de®cit referred to earlier [33].

Secondly, when children with autism were asked to imitate an unconventional action with a common object (such as drinking from a teapot) they were more likely to make errors [27]. This again provides evidence for an imitative deficit more fundamental than that expected on the basis of other known impairments. Thirdly are reversal errors [27,29]; for example,in `copying' the action of holding the hands up palm away, grasping the thumb of one hand with the other hand, autistic subjects tended to hold their palm towards themselves, recreating the hand view they had seen (sometimes also failing to grasp the thumb) instead of translating the perspective the other had seen [25]. Finally there are greater group differences with respect to sequences of actions than when single actions alone are being imitated [30]. Together, these kinds of errors suggest that deficits may be occurring in the basic ability to map actions of others onto an imitative match by oneself [29] especially when such actions are complex.

Finally,there is a curious aspect of imitation-like phenomena in relation to autism, that concerns the well-known repetitive and stereotyped behaviours and speech that may occur.These may be copied from others,including words and phrases (echolalia) and sometimes actions, that are mimicked without regard to their nor-mal goals and mea-nings. At first sight these phenomena seem contradictory to the notion of an imitative de®cit, but they may instead offer clues to the underlying neural dysfunction. We will discuss this in a later section,in integration with the findings on neurobiology to which we now turn.

4. Neurobiology of imitation

Patients with left frontal lobe lesions may show imitative dyspraxia [33,34]. These patients are unable to repeat actions performed by others, despite demonstrating
adequate motor control of their limbs. Furthermore, they are unable to replicate such gestures on a manikin [35].

This is consistent with the idea that imitation may normally rely on representation of action at a `supramodal' level [36], which is unavailable to these patients; the same lesion site will accordingly disrupt the replication of a gesture whether on the self or on another body.

Work at the neuronal level in non-human primates has started to indicate the path-ways by which representation of such actions may be built up. A number of different types of specialised neuron have been identified in the superior temporal sulcus (STS) of monkeys that are dedicated to visual processing of information about the actions of others.

Particular populations of cells code the posture or the movements of the face, limbs or whole body [37±41].Other classes of neurons appear to code movements as goal-directed actions and are sensitive to hand and body movements relative to objects or goals of the movements (e.g.reaching for,manipulating or tearing an object) [42 ± 45].

Of special relevance to our model is a subset of such action-coding neurons identi-fied in the prefrontal cortex (area F5) in monkeys [46,47]. Such neurons will fire when the monkey performs a specific action, such as a precision grip, but also when an equivalent action (a precision grip, in this example) is performed by an individual the monkey is watching. These have been called `mirror neurons' (MNs) [47]. Their po-tential relevance to imitation is signalled by another label: `monkey see, monkey do' neurons [48]. F5 cell activity, however, does not automatically lead to motor respon-ses and action performance, otherwise seeing actions performed would lead to obligatory copying (echopraxia).

The execution of actions when F5 cells are activated by the sight of actions of others, may be inhibited by mechanisms operating elsewhere in the motor pathway [49] and perhaps involving orbitofrontal cortex [50].

Although MNs cannot be studied directly in the same way in humans, the existence of a system with the properties of MNs is supported by ingenious alternative approa-ches [47, 51] including the use of transcranial magnetic stimulation (TMS) of human motor cortex to produce electromyographic potentials in muscle groups [52]. Obser-ving actions involving distal finger movements but not proximal whole arm move-ments selectively lowered the threshold for TMS to induce electromyographic activity in distal musculature.

This demonstrates input from the sight of movements to the neural system involved in motor control of the same movements.

Several functional imaging studies have noted that the sight of hand actions produ-ces activity in frontal regions (premotor cortex and Broca's area) [53,54], which may be homologous to F5 in the monkey [49]. In a recent fMRI study, activation of the left Broca's area during observation of finger movements became more intense when that same action was executed simultaneously [55]. These imaging studies also re-veal activity in parietal cortex.This area,along with possibly the superior temporal sul-cus, also shows some evidence of mirror neuron activity ([56] and M. Iacoboni (pers. com.)).

5. The functional significance of mirror neurons

MNs appear to have the capacity to embody a `supramodal representation' of action, functioning as a bridge between higher visual processing areas and motor cortex (between seeing and doing). As yet, MNs have been investigated with respect to hand actions, but it seems likely that others are concerned with different actions, such as facial expression and speech, and perhaps eye movements and the higher-level abstractions [41, 42]. However, MNs have only recently been discovered. Their precise significance is not yet known, but some specific suggestions are particularly relevant to our discussion.

5.1. Speech

Rizzolatti and Arbib [49] have suggested that the part of the monkey brain which con-tains MNs dealing with hand actions has evolved to subserve speech in humans, with language building on top of a ´prelinguistic grammar of actions' already existing in the primate brain. By acting as a bridge between perceived and performed action and speech, the MN system is thus suggested to have provided the foundations for the evolution of dialogue. Furthermore,if MNs do process auditory representations as they do visual ones,they may be important in representing the relationships between words and their speaker like the personal pronouns.

If this is true, the MN system may also provide crucial foundations ontogenetically, particularly with respect to the development of the pragmatic aspects of speech, and thence more complex aspects of language. However, not only the pragmatics of speech may depend on a functional mirror neuron system. Lack of invariance in the physical structure of phonemes gave rise to the motor theory of speech perception, which suggests that we hear sounds according to how we produce them [57, 58]. If MNs are an important link between the production and perception of speech or bet-ween sender and receiver [49]Ð then an intact MN system may be important for other stages of language development as well.

5.2. Theory of mind

Gallese and Goldman [59] have suggested that it may be possible to predict and also `retrodict' an observed person's mental state by constructing the appropriate mental correlates of an act once it is `reconstituted' in the observer's own MN system.They suggest that MN activation can permit the generation of an executive plan to perform an action like the one being watched, thereby getting the observer `into the mental shoes' of the observed (but see also Gallese [60]).

They also note this is a process that requires an ability for controlled inhibition to prevent concomitant execution of an observed action. They argue that such a mechanism is in keeping with the `simulation' model of ToM, which also requires that observed action sequences are represented in the observer ´off-line' to prevent automatic copying, as well as to facilitate further processing of this high-level social information.

5.3. More basic intersubjective phenomena:emotional contagion and shared attention

Before moving on to consider the possible role of mirror neurons in autism,it is impor- tant to note that there seems no reason in principle why MNs should not address a wide range of actions and the mental states they connote. For example,since emotio- nal states are closely linked to certain facial expressions, observation of a facial ex-pression might result in mirrored (but mainly inhibited) pre-motor activation in the ob-server and a corresponding ´retrodicted' emotional state. Such a process might help to explain the phenomenon of emotional contagion, in which people automatically mirror the postures and moods of others [61]. This seems particularly likely in view of the close connections between STS neurons, the mirror neuron circuits and the amygdala [43]. Indeed, there is direct electromyogra-phic evidence that observers adopt facial muscle activity congruent with expressions witnessed even when this process is not at an overt level [62].

Like emotion reading [20], a capacity for shared attention has been proposed as an important precursor to full theory of mind, partly on the basis of evidence that deficits in this capacity are apparent early in the life of individuals with autism, their occur-rence thus being explored as an early warning sign [16,63,64]. Here we note simply that being able to identify the focus of attention of another, or to be able to consider drawing their attention to the focus of one's own attention, is another case of being able to `stand in the other's shoes'. In shared attention, each individual's attentional focus mirrors the other, raising the prospect that MNs
could play a role in this achievement.

5.4. Imitation

In discussing the possible role of MNs in each of the above capacities, some referen-ces to imitative-like phenomena (`standing in the others shoes') have been made. It might be thought that the obvious functional role of MNs would indeed lie in imitation (in which case MN outputs would not be inhibited). However, noting that there is little evidence of imitation in monkeys [65,66] Gallese and Goldman [59] suggested that in the monkeys in which they have been identified, MNs are functioning to facilitate social understanding of others (to the extent the monkey `stands in the same `mental shoes' as the other, as Gallese and Goldman put it).

This is not argued to amount to ToM (for which there is also little evidence in monkeys [22, 23]), but it may nevertheless represent the kind of foundation which permitted the evolution of ToM in humans [59].

However, we note there is better evidence for imitation in apes than in monkeys, and of course imitation is both evident and functionally important in our own species [66, 67]. We suggest that the evolution of imitation in humans is likely to have utilised an existing MN system, even if its prior uses lay in more generalised kinds of social un-derstanding.As mentioned earlier,fMRI with human subjects during a simple imitation task did indeed find activation in area 44 as well as in parietal cortex, suggesting that the MN system is involved in imitation in humans.

If Gallese and Goldman are right about the function of MNs in monkeys, certain additional capacities had to evolve before MNs could support either imitative or more advanced ToM functions. We may guess that these additional factors reject the increased cortical volumes of great apes and humans and the representational capa-cities associated with them; their precise nature is a question for future research. For now, the critical hypothesis is that MNs provide a key foundation for the building of imitative and mindreading competencies.

Accordingly, if Rogers and Pennington were right about the linkage between imi-tation and ToM, we should, thus,expect that MNs play important roles in the whole ontogenetic cascade from early imitation to elaborated ToM. This would clearly be consistent also with Gallese and Goldmann's [59] hypothesis that MNs and ToM are linked.

6. Mirror neurons and autism

These ideas lead directly to our hypothesis that some dysfunction in the MN system might be implicated in the generation of the constellation of clinical features which constitute the autistic syndrome. The most basic hypothesis would be that there is a failure or distortion in the development of the mirror neuron system.This could be due to genetic or other endogenous causes, to external conditions adverse to MN functio-ning, or some interaction between these. Such factors might affect all MN groups or be confined to just certain groups such as those in the parietal cortex. Complete failure is not necessarily implied, for there might be merely a degree of delay or incomplete development.

Considering the factors discussed in previous sections, such dysfunction could pre-vent or interfere with imitation, or perhaps more fundamentally, lead to the `impaired formation / co-ordination of speci®c self-other representations' proposed to lie at the root of the cascade of autistic problems [21]. This in turn could explain the failure to develop reciprocal social abilities including shared/joint attention, gestural recog-nition and language (particularly the social/pragmatic aspects that Rogers and Pen-nington [21] note are the most affected), as well as breakdowns in the development of empathy and a full ToM.

Such a simple `MN-dysfunction,imitation-dysfunction' model is unlikely to provide the whole story, however, insofar as we also need to explain features of repetitive, in-exible and stereotyped behaviour and language that appears to incorporate some copying from others, in some patients with autism.

We would suggest that in fact these latter features are testimony to the per-ception-action linkage problems that occur in autism; they are consistent with the hypothesis that in autism, the mirror neuron system is as a whole malfunctioning. In these cases the system might be evidencing poor modulation.

Recall that it has been suggested that a controlled inhibitory system is essential for allowing MN's to operate `off-line' for simulation ToM to function and develop. If da-mage extends to such inhibitory components, then certain forms of mimicry might occur, yet be oddly performed.

7. Autism, executive functions and mirror neurons

In recent years it has been shown that autistic individuals experience difficulties in executive functions like planning [68 ± 72]. It tends to be assumed that executive functions such as planning ability and attentional shifting are the product of develop-mental processes largely restricted to the individual. But it is also possible that the child learns something of these functions from others, perhaps initially in relatively concrete contexts, such as playing with building bricks in infancy, and then at higher levels of abstraction and over longer time frames, such as planning meals. The initial stages in such a process might correspond to some kind of `program-level' imitation [73]. There is evidence for this in three-year-old children who are able to acquire, by imitation, alternative hierarchical plans for running off a sequence of actions to com-plete a functional task [74]. Insofar as MNs code for actions on objects, directed to-wards a goal, they could be key elements in such a process [75], helping to translate perceived executive functions into praxis and then generalising them to similar situations.

With poor MN development, the key building blocks permitting planning functions to be acquired from the external culture might be unavailable.

If mirror neurons play a part in the development of executive function as well as ToM, one would expect to see a correlation between performance on tests of each of the two abilities. This has recently been demonstrated [76]. The same principles may apply to the acquisition of other executive functions, such as approaches to problem solving and attentional shifting,which can be a problem for autistic children [68, 69]. Evidence in favour of this proposition comes from Griffiths et al. [77]. They found that apart from tests requiring rule reversal, there was no deficit of executive function in children under 4 years of age with autism. This suggests that the executive deficits are not primary but arise later on in a disrupted pattern of development. Some execu-tive functions, including inhibition and possibly visual working memory appear to be spared in autism [4,67,78,79]. These might be functions much less easily learnt by imitation.

Autistic children show not only characteristic ToM and planning deficits, but also im-pairment in reconstructing the personal past [80]. Suddendorf [81 ± 83] has proposed that the executive capacity to disengage or dissociate from one's actual current state (putting it of¯ine,as it were) in order to simulate alternative states underlies both `theo-ry of mind' and mental `time-travel' the ability to mentally construct possible (e.g.plan- ned) events in the future and reconstruct personal events from the past. Thus, in this account mirror neurons may be implied through simulation and executive functions.

8. Neuroimaging mirror neurons and `theory of mind'

If ToM and related social deficits in autism are the result of a poorly functioning sys-tem of mirror neurons, this might be manifest in recent neuroimaging studies with re-levant tasks. The mirror neuron region has been implicated in reading facial emotion in a normal population [84]. Similarly, a task that involved reading emotional expres-sions from looking at images of eyes, found that individuals with autism showed less involvement of areas normally activated during emotional interpretation, namely the left putative mirror-neuron region (BA 44/45), the superior temporal gyrus (BA 22) bi-laterally, the right insula and the left amygdala [85]. A recent review [86] of studies of both typical individuals and those with autism, seeking to identify sites active in ToM functions found that a well demarcated area of the paracingulate gyrus has been con-sistently implicated, as have areas of the anterior cingulate cortex but not the mirror neuron regions. The paracingulate gyrus and the anterior cingulate cortex are closely linked and receive dense serotonergic innervation, consistent with them performing a modulatory function and this could explain their involvement. One possible reason for the failure of these tasks to activate MN regions may be related to the control tasks that have been used. As these have been predominantly action-based such as follo-wing an action-based story, they would be expected to activate the MN regions as much as the ToM task, so discounting their apparent relevance.

9. Testing the hypothesis

From our hypothesis, several testable predictions ¯ow.

First, imitative de®cits should be apparent in autism especially where studies take place in the earliest years such as in the study by Charman et al. [87]. Particular as-pects of imitation expected to be most susceptible are those where imitation involves a co-ordinated activity between different modes of sensory input, different groups of action-coding neurons and self-other visual transformations.

Secondly, we suggest that the McGurk effect [88] whereby the perceived sound is al-tered by perceiving lip movements making a different sound,may be the result of MN functioning. In this case we predict that on testing groups of children with autism, non-standard McGurk effects will be apparent.

A third prediction can be related to the work of Baron-Cohen et al. [64] using the CHAT screening test for autism.

These authors found that joint attention at 18 months was a predictive screening item for autism (focussing on siblings of individuals with autism). Our hypothesis predicts that even earlier, appropriately-sensitive screening for an imitative deficit would be predictive in this way.

Fourth, we would predict that imaging studies will indicate altered activation of puta-tive MN regions in the brain during imitation tasks attempted by subjects with autism. Similarly, electrophysiologic studies will show altered muscle activity during the observation of actions, whether facial, vocal or with the hands

One recent study has attempted to examine mirror neurone activity in Asperger's syn-drome [89].Magnetoencephalography was used to detect a decrease in the 20 Hz ac-tivity that occurred in the MN region during median nerve stimulation whilst subjects viewed an action. The study did not find a significant difference between the five As-pergers' participants and a control group. Our analysis predicts that more extensive testing of people with autism will reveal such a difference.With the small sample size and small expected effect size (the hypothesis was tested in older individuals with the milder form of the disorder) this first study had minimal power and there was a high risk of a type two error. It is therefore important that further work is extended to larger groups with other characteristics.

10. Conclusion

The discovery of mirror neurons offers a potential neural mechanism for the imitation of actions as well as other aspects of understanding social others.

Evolution of this system may have been critical in the emergence of proto-culture and Machiavellian manoeuvring in the most encephalized non-human primates, followed by elaborate ToM and language in humans [90]. In the development of the human child, mirror neurons may be key elements facilitating the early imitation of actions, the development of language, executive function and the many components of ToM. A failure to develop an intact, sensitively regulated, mirror neuron system may therefore impair the development of these important human capabilities.

Our exploration of this hypothesis highlights numerous aspects of our ignorance.

Unanswered questions include:

1. What other cognitive and neural capacities work in conjunction with MNs to support imitation and ToM functions?

2. How do MNs relate to other social information processing neurons in performing social cognitive functions?

3. How physically extensive are MN functions which relate to autism? Do they just exist in Broca's area or are there such groups in locations such as parietal cortex, paracingulate gyrus and superior temporal sulcus?

4. Do MNs have functions in non-visual modalities as preliminary reports suggest (C. Keysers, E. Kohler, A. Umilta, V. Gallese and G. Rizzolatti, personal communication; Baker and Perrett, unpublished studies)? For example, is the sound of an action (or vocal utterance) mirrored by the same neurons as those which mirror its sight? What is the range of actions addressed by MNs?

Despite the various candidates suggested in the literature, a `prime mover' source of the complex cascade of impairments that characterise autism has so far proved elu-sive. We are suggesting that developmental delay or distortion of a mirroring system with an early age of onset could be such `prime mover'. The heterogeneity of the au-tistic condition may argue against a single cause,yet the commonalities of the clinical syndrome nevertheless permit the possibility of a core dysfunctional mechanism. If this mechanism is normally a precursor to a cascade of effects on other variable sys-tems, then its dysfunction is likely to result in a quite variable clinical picture. Our pro- posal offers such a mechanism, together with some preliminary evidence for its exis-tence and empirically testable hypotheses. If it gains further empirical support, this may suggest important new avenues for both psychological and pharmacological remediative strategies.

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[HM: Tuo "Pierret(ys)" ON SIIS "TUTKINUT" 10 VUOTTA AIKAISEMMIN PILKUL-LEEN SAMAA ONGELMAA SAMOIN KEINOIN KUN "TIETEEN MULLISTAJA" GIACOMO RIZZOLATTI, SIIS JUURI "PEILINEURONEJA" (= "AJATUS KEENIN EXPRESSIONA, PÖLHÖ-KANDEL!) - MITÄPÄ MUUTAKAAN! SAAMATTA KUI-TENKAAN ODOTETTUA TULOSTA "REHELLISESTI"! Kun homma meni havain-noissakin huijaamiseksi (eikä vain niiden tulkinnoissa), hommaan valittiin "sopiva" henkilö melko kaukaa infosota"tieteen" "esikunnasta": syntyjään neuvostoliiton-italialainen, pavlovilaisen tutkimustaustan (sen "kumottavan"!) omaava Rizzolatti Parmasta Italiasta!

[39] Perrett DI, Harries MH, Benson PJ, Chitty AJ, Mistlin AJ. Retrieval of structure from rigid and biological motion; an analysis of the visual response of neurons in the macaque temporal cortex. In: Troscianko T, Blake A, editors. AI and the eye, Chichester: J. Wiley & Sons, 1990. p. 181± 201.
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[Tosi vanha pieru: Tuo "Pierret" näyttää olevan primus motor; tuolloin ei kuitenkaan ole "tiedetty peilineuroneista"... vai "onko"? HM]



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HM: Michael Arbib oli ensimmäinen joka loikkasi ulos tuosta sisäpiiristä vaatien Rizzolattin koepöytäkirjoja julkisiksi ja näin myös antaen ymmärtää, että "kokeet" oli-vat joko väärennettyjä.Ne eivät siis olleet ryhmän jäsenillekään julkisia! Tämä tapah- tui sen jälkeen, kun ilmeni, ettei Rizzolattin "kokeita" pystytä elektrodimenetelmällä toistamaan millään lajilla. Valitettavasti Arbib siirtyi sittemmin toisen HUUHAAn, "ajattelevien tietokoneiden" pariin,eikä oikeaan tieteeseen,kuten toinen "auktoriteetti" Michael Tomasello, joka omissa kokeissaan huomasi, että IHMISAPINOILLA EI OLEKAAN MITÄÄN "MIELENTEORIAA", oletuksia toisten aikomuksista! "Sellainen" on vain ihmisellä - ihminen niitä ajatuksia ja suunnitelmia sitten olettaa muiden elä-vien päihin, perusteettomasti. Kahden hölynpölläriryhmän, "aitojen ja keinotekoisten peilineuronien, todella ajattelevien tietokneiden", ero on metodologinen: ensimmäi-nen yrittää "löytää luoonosta" oletutensa mukaisen informaatisystemminen, jälkim-mäinen taas "rakentaa sellaisen" ensin keinotekoisesti - ja sitten väitää, että "se on se, millä myös luonto toimii".


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Sari Avikainen nojaa tähän aivopieruun väitöskirjassaan 2005:


http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/avikainen/cortical.pdf


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6.1.4 Functional role of the MNS

MNS function is based, according to the direct-matching hypothesis (Rizzolatti et al. 2001), on mapping of the visual representation of an action onto the observer’s own motor representation of the same action. This matching function has been suggested to be in involved in different behaviors, such as action understanding, imitation, attri-buting mental states,and even in some aspects of language. In action understanding, the motor knowledge of the observer is used for understanding and recognizing actions of others (Rizzolatti et al.2001).In line with this as-sumption,in a PET study by Grezes et al. (1998) the premotor areas were stronger activated during observation of meaningful arm actions, when the subjects had to undertand the purpose of the actions than when they just had to imitate the actions.

The term imitation can be used to describe many kind of functions in biology, sociolo- gy and psychology. When simple defined as copying by an observer of an action per-formed by a model,the underlying neural mechanism has been proposed to be based on the MNS (Iacoboni et al. 1999; Nishitani and Hari 2000; Rizzolatti et al. 2001; Ni-shitani and Hari 2002; Wohlschläger and Bekkering 2002). The function of the MNS may involve different imitative phenomena, such as ‘res-ponse facilitation’ (an auto-matic tendency to reproduce observed movements) in-cluding release phenomena in birds and yawning, laughing and neonatal imitation in humans (Meltzoff and Moore 1977), further to higher order imitation and imitative learning (Rizzolatti et al. 2001; Wohlschläger and Bekkering 2002).

The possible role of the MNS in other complex cognitive functions, such as language (Rizzolatti and Arbib 1998) and mind-reading (Gallese and Goldman 1998), has also been discussed. In line with the motor theory of speech perception (Liberman and Mattingly 1985; Liberman and Whalen 2000), suggesting that successful linguistic communication is not dependent on sound, but rather on a neural link between the sender and the receiver that allows production of phonetic gestures, Rizzolatti and Arbib (1998) proposed that the action execution/observation mat-ching system could have served as the neural prequisite for the development of interindividual communi-cation and finally speech. Interestingly,in a recent study by Petitto et al.(2001), babies with profoundly deaf parents were shown to convey a kind of silent linguistic babling with their hand movements.

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Gallese and Goldman (1998) have proposed that the ability to detect and recognize mental states of others could have evolved from the MNS. According to one of the dominant mind-reading theories, the simulation theory (Davies and Stone 1995), other person’s mental states are detected by matching their states with resonant states of one’s own. Shared representations of different actions could serve as the basis of getting the observer into the same ‘mental shoes’ as the target (Gallese and Goldman 1998).

According to the simulation theory, all mental states requiring TOM, irrespective of whether they are are attributed to others or to oneself, should involve same neuronal system. However, in a fMRI study by Vogeley et al. (2001), modeling ones own men-tal-states activated at least in part dintinct brain regions than modeling the mental-states of others, opposed to the basic idea of simulation.

Although the relation of the MNS to different cognitive functions is still merely specu-lative, the discovery of the mirror neurons has offered a new tool to investigate brain function in our social enviroment. Future goals in this field include mapping of all brain areas involved in the mirror-neuron system and obtaining more information about their precise role in it. Futhermore,more information is needed about different stimulus types and modalities that are able to evoke mirror-neuron type activation, about the connection of the mirror-neuron system with different cognitive capacities, and about the possible role of a dysfunctional mirror-neuron system in different patient groups.

6.2 Autism

The autism spectrum disorders are a group of neurodevelopmental disorders that have a great variability in their clinical presentation but alltogether share some core symptoms, such as social impairment, deficits in communication, and restrictive pat-tern of behaviour. Autism has been a great challenge for neuroscience during the last decade.

Although a lot has been learned since the time when it was thought to be a psycho-genic syndrome caused by “refrigerator mothers”, the rapidly growing body of literature reports very heterogenous findings and theories about the basis of autism.

Abnormalities have been observed in many brain regions. However, not all subjects with autism show any abnormalities e.g. in structural or functional brain imaging, and none of the found abnormalities characterizes all subjects.In spite of the intensive re-search, we still don’t know whether autism is a single syndrome varying in severity or whether the autism spectrum of disorders have multiple etiologies that nonetheless lead into similar core symptoms.

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Autism is a rather common syndrome affecting about 0.7% of the general population of children and adolescents (Gillberg and Wing 1999). Since it is a lifelong disorder with severe deficits in social interaction and communication and since many of the subjects have psychiatric and neurologic comorbidities,there is a great need for long-term institutional, medical, educational and psycho-social care. The costs for the indi-viduals, the families and the society are significant. Even subjects at the able end of the disorder often have problems in coping independently due to the social deficits that make their every-day life difficult. Sofar the treatment in autism merely includes rehabilitation and symptomatic medication, no curative treatment exists. Although these means can of course relieve comorbid symptoms and help the subjects and families to manage in every-day life, there is evidence (Gillberg and Billstedt 2000) that the core features of autism do not change much over time. On the other hand, most of the intensive rehabili-tation has only been performed during the last decade, and randomised follow-up studies of these interventios are merely lacking. Most ef-fective results have sofar been obtained from early and highly intensive intervention programmes (Howlin et al. 1995).

6.2.1 Autism and mirror neurons

None of the cognitive theories of autism (such TOM, weak central coherence and executive function deficit) has proven to be exclusive and none has been able to explain the whole range of symptoms found in autism. Most theories focus on social symptoms, since in spite of the wide clinical variation all subjects with autism spect-rum disorders suffer from social deficits. However, the neural basis of the deficit is largely unknown.

The discovery of mirror neurons has lead to hypothesis of their role in social cog-nition (Gallese and Goldman 1998; Rizzolatti et al.2001; Williams et al.2001). Espe-cially, when evidence of the human counterpart of the monkey mirror neurons was found, a question of the possible dysfunction of the MNS in conditions associated with social impairments, such as autism, was raised. Dysfunction of the MNS could lead in impairments in imitation, action understanding and further in difficulties in using and understanding body-language, mentalising, joint attention and even some aspects of language (Williams et al. 2001).

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Total dysfunction, partial dysfunction, a dysfunction in certain parts of the MNS, or a developmental delay could all be in question.

In Studies II, V, and VI the hypothesis of possible connection between MNS and au-tism was tested. Study II showed rather normal activation of the primary motor cortex in a group of AS subjects both during observation and execution of manipulative hand actions, in spite of the deficit in their TOM abilities. The results exluded the pos-sibility of a total dysfunction of the MNS in Asperger subjects. Furthermore, no evi-dence was found of the connection between a TOM deficit and MNS dysfunction. However, the number of subjects was small (N = 5) and although no statistically sig-nificant differences were observed, a slight tendency was evident toward a weaker activation of the M1 in AS subjects.

In Study V, the AS and HFA subjects’ imitation abilities were examined by using a behavioural task. Recent evidence suggests that human imitation is based on the mirror-neuron system (Iacoboni et al. 1999; Nishitani and Hari 2000; Wohlschläger and Bekkering 2002). Normally people tend to imitate as in looking at a mirror (Bek-kering et al. 2000; Iacoboni et al. 2001) and observation of movements in a mirror-image view speeds up performance also in non-imitative tasks (Brass et al. 2000; Brass et al. 2001).

However, Study V showed that AS and HFA subjects are impaired in goal-directed imitation, when the imitation occurs in a mirror-image fashion. As certain aspects of imitation, such as imitation requiring self-other visual transformations, are most susceptible for MNS function (Williams et al. 2001), a developmental delay or adysfunction of the MNS could explain the observed results.

In Study VI, the hypothesis of a MNS dysfunction in autism was tested further by re-cording cortical activations while AS subjects imitated orofacial gestures. The results showed abnormal activation in the IF and M1 areas. As the the human mirror-neuron areas (the inferior parietal region, the Broca’s region and the M1) are activated in se-quence, dysfunction of both frontal and parietal part of the MNS could explain the de-layed and weaker activation of the IF and M1 areas. Broca’s region, the homologue of monkey F5 area, is activated during observation, exe-cution and imitation of hand and mouth movements (Iacoboni et al.1999; Nishitani and Hari 2000; Nishitani and Hari 2002) and considered as an essential part of the human MNS. Dysfunction of the IF part of the MNS could affect social abilities via connections to the orbitofrontal cortex and to the anterior ventral medial frontal region that are considered to contribute to theory of mind.

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The STS region is closely connected to the MNS function and it has an important role in perception of many kind of socially relevant visual stimuli (for a review, see Allison et al. 2000; Puce and Perrett 2003). Interestigly, the STS region is also activated in tasks requiring mentalising (McGuire et al. 1996; Gallagher et al. 2000). In line with these results, autistic children, have been shown to be impaired in visual recognition of biological motion (Blake et al. 2003). In a PET study by Castelli et al. (2000), acti-vations of the STS and medial prefrontal cortex were weaker in autistic than in cont-rol subjects during a mentalising task, whereas the activity of the exstrastriate corti-ces did not differ from the controls. However,in Study VI activation of the occipital and STS areas did not differ between AS and control subjects. This discrepancy probably reflects different activation cascades within the STS region; perception of an mouth and hand actions in order to imitate might be intact in the STS level in AS subjects, whereas processing of more abstract and complex social stimuli (such as cartoons and stories of TOM) could be affected. Accordingly, perception of goal-directed hand actions was found to activate the caudal STS and the intraparietal sulcus, whereas perception of expressive whole-body motion activated the rostrocaudal STS, as well as the limbic structures, including the amygdala (Bonda et al. 1996).

Subjects in Studies II, V, and VI were adults and had AS (except one subject in Study II and two subjects in Study V who were autistic) representing the able end of the au-tism spectrum disorders. This subject group was chosen, since MEG re-cordings req-uire some co-operation from the subjects, especially when tasks in-volve active parti-cipation. Additionally, the subjects have to keep their heads stea-dy during the mea-surement to avoid movement artefacts and to enable identification of accurate source locations. Futhermore,in the AS group the amount of other factors that could affect the results, such as medication, comorbidities and language problems, is at minimum. Adult subjects were studied, because the knowledge of MEG responses in children and adolescents is still rather limited. However, in adults with the most “mildest” form of the disorder, the size of the effect could be smaller than in more severely affected subjects. On the other hand, although most AS and high-functioning autistic subjects, are of normal intelligence, they suffer from social difficulties, which according to the MNS hypothesis are just the symptoms that are linked with the MNS function.

Altogether, the results from Studies II and VI suggest that MNS dysfunction can account for a part of the imitation and social impairments in subjects with Asperger’s syndrome.

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Since we only studied able adult subjects, it would be interesting in the future to exa-mine MNS function in more affected and younger subjects. Furthermore, modulatory influences from the prefrontal theory-of-mind regions on the MNS should be evaluated.

In autism research, lack of replication of studies, small and heterogenous experimen- tal groups and poor control of other confounding variables have for long been a prob-lem, therefore future studies should attempt to investigate more homogeneous sub-groups within the autism spectrum disorders. Effective communication between reseachers on this field will help to integrate and update the diagnostic criteria for the different subgroups. The studies should also aim at integrating in-formation from dif-ferent fields of the research, such as genetics,functional imaging and neuropsycholo- gy. Hopefully, in the near future we are able to understand much better the biological mechanisms underlying the mystery of autism.

...


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[HM: Rizzo puhuu "suupeilineuroneista" jo 1981, 15 vuotta ennen "yllättäviä peilineuronilöytöjä"...]

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https://www.cell.com/trends/cognitive-sciences/abstract/S1364-6613(04)00024-5

FOXP2 and the mirror system


Abstract

An inherited deficit in spoken language has been associated with a mutation in the forkhead box P2 ( FOXP2) gene on chromosome 7. A recent functional magnetic resonance imaging study has linked the deficit to underactivity in Broca's area during word generation, which in turn suggests a possible link between FOXP2 and the mirror-neuron system observed in the primate homologue of Broca's area. This link might have implications for the evolution of Broca's area and its role in speech.

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Article Info

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DOI: 10.1016/j.tics.2004.01.007

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https://phys.org/news/2009-05-humanized-mice-volumes.html


Why can we talk? 'Humanized' mice speak volumes

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Read more at: https://phys.org/news/2009-05-humanized-mice-volumes.html#jCp
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Read more at: https://phys.org/news/2009-05-humanized-mice-volumes.html#jCp
Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.

Read more at: https://phys.org/news/2009-05-humanized-mice-volumes.html#jCp

Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.


"In the last decade or so, we've come to realize that the mouse is really similar to hu-mans," said Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropolo-gy. "The genes are essentially the same and they also work similarly." Because of that, scientists have learned a tremendous amount about the biology of human diseases by studying mice.

"With this study, we get the first glimpse that mice can be used to study not only disease, but also our own history."

Enard said his team is generally interested in the genomic differences that set humans apart from their primate relatives. One important difference between humans and chimpanzees they have studied are two amino acid substitutions in FOXP2. Those changes became fixed after the human lineage split from chimpanzees and earlier studies have yielded evidence that the gene underwent positive selection. That evolutionary change is thought to reflect selection for some important aspects of speech and language.


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https://reader.elsevier.com/reader/sd/7DE13466AC245BB500CFA9E5BF4B0D7CA9B77A5497E0CAB7195C2E30C95A4DF34AA279646AED38680CED4D2443079BED


Article

No Evidence for Recent Selection at FOXP2 among Diverse Human Populations Graphical

Sohini Ramachandran et. al.

No support for positive selection at FOXP2 in large genomic datasets.

Sample composition and genomic scale significantly affect

An intronic ROI within FOXP2 is expressed in human brain cells and cortical tissue

This ROI contains a large amount of constrained, human-specific polymorphisms


Ingressin viitteet




" J. exp. Biol. 146, 87-113 (1989)

87 Printed in Great Britain © The Company of Biologists Limited 1989

FRAMEWORKS OF ANALYSIS FOR THE NEURAL REPRE-SENTATION OF ANIMATE OBJECTS AND ACTIONS BY D. I. PERRETT, M. H. HARRIES, R. BEVAN, S. THOMAS, P. J. BENSON, A.J. MISTLIN, A. J. CHTTTY, J. K. HIETANEN AND J. E. ORTEGA

Department of Psychology, University of St Andrews, St Andrews, Fife KY16 9JU, Scotland

Summary

A variety
of cell types exist in the temporal cortex providing high-level visual descriptions of bodies and their movements. We have investiga-ted the sensitivity of such cells to different viewing conditions to de-termine the frame(s) of reference utilized in processing. The respon-ses of the majority of cells in the upper bank ofthe superior temporal sulcus (areas TPO and PGa) found to be sensitive to staticand dyna-mic information about the body were selective for one perspective view (e.g. right profile, reaching right or walking left). These cells can be considered toprovide viewer-centred descriptions because they depend on the observer's vantage point. Viewer-centred descriptions could be used in guiding behaviour. They could also be used as an in-termediate step for establishing view-independent responses of other cell types which responded to many or all perspective views selective-ly of the same object (e.g. head) or movement. These cells have the properties of object-centred descriptions, where the object viewed provides theframe of reference for describing the disposition of object parts and movements (e.g. head on top of shoulders, reaching across the body, walking forward 'following the nose'). For some cells in the lower bank of the superior temporal sulcus (area TEa) the responses to body movements were related to the object orgoal of the move-ments (e.g. reaching for or walking towards a specific place). This goal-centred sensitivity to interaction allowed the cells to be selective-ly activatedin situations where human subjects would attribute causal and intentionalrelationships.

Introduction

This paper describes the response properties of cells in different re-gions of thetemporal association cortex of the macaque monkey. It is the aim of the paper to summarize the sensitivity of cells in this brain area to different types of biologically important visual stimuli. A paral-lel aim is to consider frameworks for visual processing which are ap-propriate for making explicit different types of informationabout ani-mate objects and hence for achieving a more complete understanding ofthe world.

Key words: temporal cortex, single cell, face, action.

88 D.I. PERRETT AND OTHERS

The first section of the paper focuses on cells in one region of the higher-association cortex (the upper bank of the superior temporal sulcus, areas TPO and PGa of Seltzer & Pandya, 1978; Pandya & Yeterian, 1985) which appear to beinvolved in the re-cognition of individuals (Fig. 1,left column) and how these indi- viduals are moving (Perrett etal. 1985a, b; Baylis et al. 1985).

This region has received extensive study since it was realised that it contained cells selectivelyre sponsive to faces (Bruce et al. 1981; Perrett et al. 1982,1984,1987; Rolls, 1984; Desimone etal. 1984; Mikami & Nakamura, 1988). The second section focuses oncoding in an adjacent section of cortex in the lower bank of the same sulcus (area TEa of Seltzer & Pandya, 1978).

Populations of cells in this region appear to be involved in the recognition of actions, that is, how other individuals are inter-acting with the environment (Fig. 1, middle column). Studies of action coding have beenmainly restricted to actions of the hand but there are indications that the framework for such proces-sing applies to actions of the whole body (Perrett et al.1989a, b, e).

Physiological methods

Standard single-unit recording techniques were employed to study cells indifferent regions of the temporal cortex of awake, behaving rhesus macaquemonkeys (for details see Perrett et al. 1985a,b). A large-aperture shutter was usedto present different types of visual stimuli. These included real faces and bodies, two-dimensional slides of monkeys and humans in different pos-tures,videotapes of different actions and a variety of simple and complex three-dimensional stimuli. Responses to these stimuli were measured by analysing the number of actionpotentials from individual cells in a 0-25 s period beginning 100 ms after the shutteropened. This period of analysis was chosen because it is relatively uncontaminated with eye movements and visual responses in the temporal cortex generally havelatencies greater than 100 ms.Viewer- and object-centred descriptions

General characteristics of face

Within the cortex of the superior temporal sulcus (STS) popu-lations of cellshave been studied that respond more to the sight of faces than to a variety ofsimple stimuli (e.g. bars or gratings) or complex, potentially arousing stimuli (e.g.hands, bananas, pictures of snakes and birds of prey) (Bruce et al. 1981; Penett etal. 1982). Most such cells are sensitive to the general charac-teristics of faces andrespond to a variety of faces regardless of their species (human or monkey). Thesecells also show a remar-kable tolerance for changes in viewing conditions andrespond to faces despite change in retinal size, orientation and position (Perrett etal. 1982, 1984, 1988, 1989d; Bruce et al. 1981; Rolls & Baylis, 1986). This generalization indicates that the cells' discriminative responses to faces are notdependent directly on simple visual attributes (e.g. position and orientation oflocal ed-ges, spatial frequency components) which change from display to display.
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Publications (11)

Measurements were made of the way human subjects visually inspected an idea-lized machined tool part (a 'widget') while learning the three-dimensional shape of the object. Subjects were free to rotate the object about any axis. Inspection was not evenly distributed across all views. Subjects focused on views where the faces of the object were orthogonal to the line of sight and the edges of the object were aligned parallel or at right angles to the gravitational axis. These 'face' or 'plan' views were also the easiest for subjects to bring to mind in a mental imagery task. By contrast, when subjects were instructed to imagine the views displaying the most structural information they visualized views lying midway between face views.
An investigation was made into the sensitivity of cells in the macaque superior tem-poral sulcus (STS) to the sight of different perspective views of the head.This allowed assessment of (a) whether coding was 'viewer-centred' (view specific) or 'object-cen-tred' (view invariant) and (b) whether viewer-centred cells were preferentially tuned to 'characteristic' views of the head. The majority of cells (110) were found to be viewer-centred and exhibited unimodal tuning to one view. 5 cells displayed object-centred coding responding equally to all views of the head. A further 5 cells showed 'mixed' properties,responding to all views of the head but also discriminating between views. 6 out of 56 viewer and object-centred cells exhibited selectivity for face identity or species. Tuning to view varied in sharpness. For most (54/73) cells the angle of per-spective rotation reducing response to half maximal was 45-70 degrees but for 19/73 it was greater than 90 degrees. More cells were optimally tuned to characteristic views of the head (the full face or profile) than to other views. Some cells were, how-ever, found tuned to intermediate views throughout the full 360 degree range. This coding of many distinct head views may have a role in the analysis of social signals based on the interpretation of the direction of other individuals' attention.
The importance of different perspective views for the recognition of model heads was studied.

In experiment 1 subjects were instructed to learn the appearance of six heads placed individually on a turntable free to rotate through 360 degrees. Subjects did not distri-bute their time evenly but focussed their inspection on particular views (the full face view and a view close to the profile).Despite differential inspection of these two views during the learning phase, the face, half profile, and profile views were recognized with equal efficiency in a subsequent recognition task with static views.

Experiment 2 used the inspection paradigm to investigate view preference during the recognition of heads from memory. In this experiment subjects were asked to learn the appearance of three heads each seen rotating at an even speed. In a subsequent retrieval task the subjects actively inspected six model heads on the turntable and were asked to differentiate the three heads previously seen rotating from three novel heads. The pattern of inspection in this retrieval task was equivalent to that in experi-ment 1. Results suggest that during the encoding into memory subjects construct descriptions of specific prototypical views of the head and that descriptions of these same views are preferentially utilised during recognition.
Physiological recordings along the length of the upper bank of the superior temporal sulcus (STS) revealed cells each of which was selectively responsive to a particular view of the head and body. Such cells were grouped in large patches 3-4 mm across. The patches were separated by regions of cortex containing cells responsive to other stimuli. The distribution of cells projecting from temporal cortex to the posterior regions of the inferior parietal lobe was studied with retrogradely transported fluores-cent dyes. A strong temporoparietal projection was found originating from the upper bank of the STS. Cells projecting to the parietal cortex occurred in large patches or bands. The size and periodicity of modules defined through anatomical connections matched the functional subdivisions of the STS cortex involved in face processing evident in physiological recordings. It is speculated that the temporoparietal pro-jections could provide a route through which temporal lobe analysis of facial signals about the direction of others' attention can be passed to parietal systems concerned with spatial awareness.
Conducted 2 experiments that examined the behavioral significance of tactile and motion sensitive cells in the superior temporal sulcus (STS) of the macaque brain. In the awake, behaving monkey ,the critical dimension for polymodal coding was whether or not the sensations were expected. Tactile stimulation out of sight could not be predicted and elicited neuronal responses. By contrast, when the monkey could see and, therefore, predict impending contact, or when the monkey touched a familiar surface in a predictable location, cell responses were reduced or abolished. In an analogous way some cells were unresponsive to the sight of the monkey's own limbs moving, but responded to the sight of other moving stimuli.
(PsycINFO Database Record (c) 2012 APA, all rights reserved)
we have suggested that there are three ways in which body movements are classi-fied by nerve cells in the temporal lobe / by referring the movements to three different frames of reference, the viewer, the object viewed or the goal of an action,in this clas- sification a comprehensive understanding of the nature and intention of movement can be derived (PsycINFO Database Record (c) 2012 APA, all rights reserved)
A variety of cell types exist in the temporal cortex providing high-level visual descrip-tions of bodies and their movements. We have investigated the sensitivity of such cells to different viewing conditions to determine the frame(s) of reference utilized in processing. The responses of the majority of cells in the upper bank of the superior temporal sulcus (areas TPO and PGa) found to be sensitive to static and dynamic information about the body were selective for one perspective view (e.g. right profile, reaching right or walking left). These cells can be considered to provide viewer-centred descriptions because they depend on the observer's vantage point. Viewer-centred descriptions could be used in guiding behaviour. They could also be used as an intermediate step for establishing view-independent responses of other cell types which responded to many or all perspective views selectively of the same object (e.g. head) or movement. These cells have the properties of object-centred descriptions, where the object viewed provides the frame of reference for describing the dispo-sition of object parts and movements (e.g. head on top of shoulders, reaching across the body, walking forward 'following the nose'). For some cells in the lower bank of the superior temporal sulcus (area TEa) the responses to body movements were related to the object or goal of the movements (e.g. reaching for or walking towards a specific place). This goal-centred sensitivity to interaction allowed the cells to be selectively activated in situations where human subjects would attribute causal and intentional relationships.
Experimental and clinical studies have generally shown that the neural mechanisms for face processing in man are (1) designed to deal with the configuration of upright faces and (2) located predominantly in the right cerebral hemisphere. Monkeys would seem to process faces in a different manner to humans since they appear to show no hemispheric asymmetry and to treat upright and inverted faces equivalently. We re-examine these claims. Our reaction time studies reveal that monkeys do behave like human subjects since they process facial configuration faster when stimuli are pre-sented upright as compared with horizontal or inverted. Single unit studies in the monkey reveal patches of neurones responsive to faces in the upper bank and fun-dus of the left superior temporal sulcus (STS). Recording from the right hemisphere also reveals cells responsive to faces but in this hemisphere such cells appear less numerous. These cells process upright faces faster than inverted faces. Face proces-sing in monkeys and man appears to utilize qualitatively similar mechanisms, but the extent and/or direction of cerebral asymmetry in these mechanisms may not be similar.
The way in which human subjects distribute their time when attempting to learn the surface appearance of objects placed on a stand free to rotate about its vertical axis was investigated. Experiments were undertaken to establish whether observers con-centrate their time on particular views and, if so, to determine the image characteris-tics of the preferred views. For tetrahedra, subjects concentrated on views which pre-sented a face or an edge centred on the line of sight. Both of these views were sym-metric about the vertical axis. For potatoes as examples of opaque smooth objects, subjects concentrated on four views in which the object's principal (long) axis was oriented side-on or end-on to their line of sight. For such views the horizontal width (and surface area) of the object's image had maximum and minimum values. Preferred views were not systematically related to views defined as stable from the appearance of surface boundaries or 'singularities'.

Citations (1,297)

... This region has been associated with visual-spatial attention, in particular atten-tional shifts (Corbetta, 1998; Corbetta et al., 1995; Haxby et al., 1994). Further, tem-poral-parietal connections may play a role in transferring expressive, changeable fa-cial features (e.g.,facial expressions,gaze directions) from the temporal to the parietal regions for spatial attention (Harries and Perrett, 1991). This might partially explain the difference noted between the parietal ROI and the occipito-temporal ROI. ...


... They found that their participants spent time exploring "plan" views, namely views that were on-axis or orthogonal and parallel to the object's structural axis. Perrett et al. [10,11] found a similar preference for "plan" views in tool-like as well as "novel" objects. The mixed evidence could be due to the fact that view-canonicity can be ex-pressed by the multiple factors [12]: goodness for recognition (a good view for recog-nition shows the most salient and significant features, and it is stable with respect to small transformations, and it avoids a high number of occluded features), familiarity (recognition is influenced by the views that are encountered more frequently and during the initial learning), functionality (recognition is influenced by the views that are most relevant for how we interact with an object), and aesthetic criteria (preferred views can be influenced by geometric proportions). ...


... First, the task demand and stimuli used in prior studies might be critical in the ob-servation of this deficit. In line with this claim, abnormal processing of gaze direction has been reported in both acquired and developmental prosopagnosia in studies using face pictures with a deviated head orientation faces (McConachie,1976; Perrett et al., 1988;De Haan & Campbell,1991) but not with a frontal head orientation (as in Duchaine et al.,2009;Burra et al.,2017). In addition,despite being able to discriminate gaze direction explicitly (left, right, center), prosopagnosia patients failed to respond automatically to gaze direction (Burra, Kerzel, & Ramon, 2017). ...


... These findings suggest that facial information from the subcortical system might af-fect the cortical visual system in early infants with premature cortical visual systems. Furthermore, previous behavioral studies have reported that monkeys and humans display behavioral sensitivity to face orientations (Perrett et al., 1990) and that great apes follow the directions of a human experimenter based mainly on the human's face orientation with eye direction also playing a role (Tomasello et al., 2007). These findings suggest that frontal faces with their face orientation directed to the subjects are important social signals regardless of gaze direction. ...


... Perception of 3D orientation has been systematically studied for objects and faces. For example,rigid 3D objects and faces can be best recognized from canonical views (Blanz, Tarr & Bülthoff,1999), and humans tend to choose preferred views when lear-ning 3D objects and faces (Harries, Perrett, & Lavender, 1991; Peissig & Tarr, 2006; Perrett & Harries, 1988). It has also been shown that local and global strategies are combined in a flexible manner when judging the facing in depth of 3D objects (Foster & Gilson, 2002; Troje & B ¨ulthoff, 1996; Watson, Johnston, Hill, & Troje, 2005). ...

... We localized OFA in the lateral inferior occipital gyrus ( Gauthier et al., 2000), FFA in the mid-fusiform gyrus ( Kanwisher et al., 1997;McCarthy et al., 2003), and STS in the posterior part of the superior temporal sulcus. Since studies reported differences in face processing mechanisms across hemispheres ( Perrett et al., 1988;Kanwisher et al., 1997;Ishai et al., 1999;Haxby et al., 2000;Rossion et al., 2003;Kanwisher and Yovel, 2006;Meng et al., 2012), we defined face-sensitive areas separately for each hemisphere to assess differences in activation between the two hemispheres. ...


... They found that their participants spent time exploring "plan" views, namely views that were on-axis or orthogonal and parallel to the object's structural axis. Perrett et al. [10,11] found a similar preference for "plan" views in tool-like as well as "novel" objects. The mixed evidence could be due to the fact that view-canonicity can be ex-pressed by the multiple factors [12]: goodness for recognition (a good view for recog-nition shows the most salient and significant features, and it is stable with respect to small transformations, and it avoids a high number of occluded features), familiarity (recognition is influenced by the views that are encountered more frequently and during the initial learning), functionality (recognition is influenced by the views that are most relevant for how we interact with an object), and aesthetic criteria (preferred views can be influenced by geometric proportions). ...


... The shapes and the parameters of each tuning curve are usually de- pendent on the specific neuron and stimulus. We highlight the work performed by Perret et al. in [79] and the work of Newsome and Salzman in [80] that investigated the firing patterns in reaching motions, and which we base our work upon. We extracted their results and used the func- tions they proposed in designing our Gaussian functions within the population are defined. ...


... Additional mirror neurons were later found within monkey parietal regions, which innervate the premotor cortex (Gallese, Fadiga, Fogassi, & Rizzolatti, 2002). With the incorporation of superior temporal re- gions, which are involved in recognizing biolo-gical motion (Perrett et al., 1990) and are reciprocally connected to parietal regions, a putative macaque imitation system has emerged Gallese et al., 1996). However, one significant limitation of the mirror neuron system model of imitation in macaque mon-keys is the simple fact that the available data indicate that the imitative abilities of species within this genus are notably limited (Visalberghi & Fragaszy, 2002). ...

... The interest in the brain networks underlying others' observed action processing has been triggered by the discovery, in the monkey ventral premotor area F5, of the so-called "mirror neu- rons," which respond during both action execution and others' action observation (di Pellegrino et al.1992;Gallese et al. 1996;Rizzolatti et al. 1996). This finding demonstrated that observed action processing is not limited to visual brain areas (Perrett et al. 1989; Vangeneugden et al. 2009; Singer and Sheinberg 2010), but involves frontoparietal areas belonging to the motor system as well (see Materials and Methods for the anatomo- functional criteria defining the areas of inte-rest). Subsequently, neurons responding to the observation of another individual's action have been described in 2 parietal areas: PFG, in the infe- rior parietal lobule (IPL) convexity ( Fogassi et al. 2005;Rozzi et al. 2008;Bonini et al. 2010) and the anterior intraparietal (AIP) area ( Pani et al. 2014;Maeda et al. 2015). ...



RK
16.06.2005 01:47:09
176429

Rizzolattin "peiliSOLUhavaintoja" ei ole pystytty vahvistamaan.

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

Harmaa.Eminenssi kirjoitti 12.06.2005 (176090)...

>Tällaista keskustelua aiheesta muualla:

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

RK (176097): Antipavlovistikirkon sisäistä jargoonia.

Mutta ERITTÄIN MIELENKIINTOISTA heti ensimmäisessä jutussa,että nimenomaan SOLUTASON ilmiöitä (ehdollistuneita tai muita) EI OLE EDES HAVAITTU muualla kuin Rizzolatti makaki-apinoilla!

Ja itse asiassa, kaikki muu tohina huomioiden tuon asian ympärillä, SIIHENKÄÄN "HAVAINTOON" EI TAIDA OLLA KAUHEASTI LUOTTAMISTA!

Arbib myös pulputtaa kovasti matkimisesta apinoilla,ja löytää siihen alkeellisilla api-noilla rudimentaarisen ehdottoman (tai leimaus-) refleksinkin, VAIKKA "PEILISOLU-TEORIAN" ISÄT Goldmann ja Gallese kategorisesti "KIELTÄVÄT" MATKIMISILMIÖIDEN OLEMASSAOLON apinoilla ja laajemminkin luonnossa” :

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/175827?page=1#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 ima-ging 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. “

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 tunnis-tamiselle ja oppimisella, jotka eivät TARVITSE YHTÄÄN SE ENEMPÄÄ ainakaan geneettisiä ”PEILISYSTEEMEITÄ” kuin ”-SOLUJAKAAN”:

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/162827?page=1#162827

Kuten Arbibkin tavallista rehellisempänä sosiobiologistina aiheellisesti mainitsee.

” ) In computer science and engineering, simulation involves the ability to predict a trajectory in quantitative 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. “

Olen jossakin hieman erheellisesti maininnut, että ehdollistumisteorian mukainen mielenteoria kuuluu ”peilisolu- / -systeemiteoreetikkojen” kategoriaan ”simulaatioteoriat” (enemmänkin kuin Goldmannin kategoriaan ”teoriateoriat”).

Nyt niillä on kuitenkin uusi kategoria ”luokitteluteoria” (classification theory), johon se vasta istuukin hyvin, esimerkkinä juuri pähkinänkuoren rikkomisprodeduuri, joka ak-tivoituu myös rikkontuvan pähkinänkuoren aiheuttamasta äänestä,eikä vain sellaisen työn tekemisestä tai katselemisesta! (Itse asiassa siitä on vain yksi kukonaskel sym-bolifunktioon, että pähkinänkuoren rikkomisääni yhdistetään johonkin kellonkilauk-seen, 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. “

Arbib erehtyy siinä, että tuo refleksin aktivoituminen toiminnan äänestä ei olenkaan liittyisi YMMÄRTÄMISEEN: 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 aiheuttaa 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. ”

“Peilisolusta” pidetään kuitenkin kiinni kuin sika limpusta, vaikka sitä EI TARVITA MIHINKÄÄN, ja HAVAINTOKIN niistä on asetettu kyseenalaiseksi! Lisäksi kehitel-lään uusia stiiknafuuliota, kuten ”kvasipeilisoluja” (jotka aktivoituvat havaitessa, mutta eivät tehdessä)!

SENKÖ TÄYTISEEN tarvitaan (vielä lisää) tuollaisia VALEKÄSITTEITÄ, se alkupe-räinen ”peilisolun” valekäsite oli fysiologisesti tarpeeton, koska jokainen aivokuoren pinnan solu olisi sen mukaan ainakin jonkin asian ”peilisolu”, mutta tuo ”kvasipeiliso- lu” on jo LOOGISESTIKIN saman tason "käsite" kuin vanhaa lasten vitsiä lainatakse-ni ”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. “

OLOSUHTEET HUOMIOON OTTAEN: terävästi päätelty…: on pidettävä erillään se, mitä tulokset kertovat, ja mitä "me" (="sosiobiologistikirkko") HALUAMME USKOA niiden tarkoittavan!

Ei käynyt niin kuin pikku Kallelle, kun USKONNON opettaja kysyi, että "mikä on rus-kea 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 yodennäköisyystasolla ovat ehdollistumisteorian (”orava”) ja ”peilisolutoerian” (”Jeesus-lapsi”) edustamat tulkinnat neurofysiologisista kokeista….)

” 6) [Gerely] 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.”

MITEN tuo on muka “peilisoluteorian” vastahypoteesi?

Jos siellä ”peilisolussa” on jokin TOIMINTA koodattuna, niin sehän on sitä juuri ”toimenpiteiden seurantona”, miten se muuten siellä voisi olla?

Mutta helvetin paljon yksinkertaisemmin tuollainen selittyy ehdollistumisteorialla ja ILMAN SOLUTASON KOODAUSTA, koska kullakin niillä osatoiminnoilla voi olla ja on oma refleksikaarensa SAMASSA "PROSESORISSA", ja niiden välille tarvitaan vain järjestävä yhteys, jotta niistä saadaan ”koko toiminnan refleksikaari” seurantoi-neen! Tuohon viime mainittuun voi sitten ärsykkenä viitata sana tai vaikka pähkinän-kuoren tietynlainen risahdus apinan salavarastolla. Tämä on sitä ehdollisten reflek-sien SYSTEEMISYYTTÄ, että ”ylin” ja ”abstraktein” taso määrää, ja ohjaa hierarki-sesti niihin alempiin , perustavampiin, alkupeäisempiin. Sellaista ei esiinny genetti-sillä erillisillä ehdoTTOMilla reflekseillä, 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 originaalinen 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 simu-lation theorist must explain how the same neural circuitry could support the simula-tions 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. “

Tässäkään ei ole ehdollistumisteorian valossa mitään ihmellistä: kaksi eri toimintoa voi hyödyntää yhtä aikaa samaa aktivoitua refleksikaarta, siitä on usein vain hyötyä, jos se on muutakin kautta aktiivisena (sanotaan vaikka bändisoitossa tai pariluiste-lussa, missä on toisella silmällä tai korvalla seurattava naapureiden suoritusta, tuol-lainen 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 erehdykdessä 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 extended to "mirror systems" by analogy and terminology. As Arbib notes, there is no evidence supporting this claim. “

Ilman “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 essen-tial features of the 'simulation' theory." Yes, it does - it loses its main point. If an action is 'classified' without simulation, 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.

“Simulaatioteorialla” voi pyyhkäistä tiettyä paikkaa ”luokitteluteorian” hyväksi, ja saman tien ”automaattisella mielenlukemisella”.

Jos esiintyy ”simuloivaa mielenlukemista” se on yhteisen harjoittelun tulos jossakin useamman henkilön työ- tmv. prosessissa. Ja se koskee pelkästään sitä tiettyä, yhteistä suoritusta edellyttävää prosessia.

Seuraavat pykälää kovempien "peisoluteorian" kannatajien "kriittiset kommentit" näistä osin kerettiläisistä huomiosta ovat mielenkiintoista paljastavaa luettavaa "peilisolutoerian" kannalta...

Pätkaisen tähän tällä kertaa, ja palaanniihin tuonnempana, inshallah...

RK


Arbibin Wiki-sivulla mainitaan hänen roollinsa Rizzolattin "peilineurooniryhmässä", MUTTA EI PUHUTA MITÄÄN HÄNEN KYLMISTÄ JÄLKIKÄTEISTERVEISISTÄÄN SILLE!

" With Richard Didday, he developed one of the first winner-take-all neural networks in 1970. More recently, with Giacomo Rizzolatti, the leader of research team that discovered mirror neurons, he proposed an evolutionary link between mirror neurons, imitation, and the evolution of language. "


Vieläkin kaemmaksi rikostutkinassa päästään:

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/150509?page=1#150670

RK
14.09.2004 00:11:10
150670

Re: perustosiasiat, "peilisolut" on jo 1968 hahmoteltua poliittista "eurotiedettä

H5 kirjoitti 12.09.2004 (150560)...

>Hyvä RK

>Tietääkseni ainakaan missään neurologisissa julkaisuissa ei ole vielä >nimenomaisesti väitetty että ns. peilisolut olisivat rakenteeltaan mitenkään erilaisia >muista saman alueen (F5) soluista ts. nimenomaan tiettyjen geenien aktivoituminen >juuri näissä neuroneissa tekisi niistä peilisoluja. Kerro jos tiedät jotain muuta.

“Peilisolun” käsite on kopioitu kritiikittömästi Rizzolattilta, ja sitä pidetään apinoilla ”todistettuna”, vaikka Rizzolatti ei mitään sellaista ole todistanut (ja aivan tarkasti ottaen ei niin edes välitä tehneensä):

http://www.cercor.oupjournals.org/cgi/content/full/12/8/847

“PeiliSOLUUN”,siis mineomaan SOLUUN eikä esimerkiksi hermokudoksen synapsi- yhteyksiin, on muka ”koodattuna toimintaa” (tarkasti ottaen käytetään ilmausta ”solun koodaamaa”, kuin se olisi jokin ”itsenäinen subjekti”, äärimmäisen sekavaa ja epä-määräistä kielenkäyttöä, kuten näissä yhteyksissä tavaksi on tullut, muistettakoon vain vaikkapa Tooby&Cosmidesin houru ”EP Primer):

“ Within area F5 there is a class of neurons, known as mirror neurons, that respond to the sight of another monkey or experimenter performing the same type of action encoded by that neuron (Di Pellegrino et al., 1992 ; Rizzolatti et al., 1996a ). “

Erittäin kummallista jopa “evoluutiopsykologiankin teorian” kannalta tässä yhteydes- sä on että ”KYKY ON KEHITTÄNYT” sen (”pienen” , ”spesialisoituneen” á la Tooby & Cosmides) ”laitteen”, JOLLE SE ITSE KYKY SITTEN KUITENKIN PERUSTUU (ei-vätkä ne OLEKAAN ”kehittyneet yhdessä” evoluutiossa, kuten sisnsä houru T&C:kin edelyttäisi:

“ Mirror neurons are characterized by their response to both observation and execution of the same action. It has been proposed that the ***human ability to imitate evolved out of the mirror system***, with its capacity to match directly observed and executed actions (Arbib, 2002 ). !

Jossakin on nyt matoja jopa “E.P::nkin kannalta…tieteestä puhumattakaan. >:-]

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0V-3T70Y2D-4&_coverDate=05%2F01%2F1998&_alid=200452853&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4872&_sort=d&view=c&_acct=C000049137&_version=1&_urlVersion=0&_userid=950195&md5=cdf2ec9c552db02dce5a31201b9465d2

Ja täältä sitten löytyvät ne ankarat antipavlovistit Chomskyt ja Pinkerit, joiden tuotanosta voi haulla etsiä nimeltä asiantuntevaa keskustelua tältäkin palstalta.

57. N. Chomsky. Knowledge of Language: Its Nature, Origin and Use, Praeger (1986).

59. S. Pinker and P. Bloom. Behav. Brain Sci. 12 (1990), pp. 707–784. Abstract-PsycINFO | $Order Document

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WVC-446CP4R-39C&_user=950195&_coverDate=01%2F01%2F1900&_fmt=summary&_orig=search&_qd=1&_cdi=7099&view=c&_acct=C000049137&_version=1&_urlVersion=0&_userid=950195&md5=50b3f03e9e80a80357dede88fcbd7aac&ref=full

Rizzolattin ja “peilisoluteorian” takana on EU:n jo 1968 organisoima sosiobiologisti-nen seura, jonka ssäntöjenmukaisena toimenkuvana on edistää ”aivolaitteiden (mechanism) ja käyttäytymisen suhteiden tutkimusta”.

Joten ”huippututkijoita” riittää kehuskelemaan toistensa ”löytöjä”…

Eivär ne ”pienet evoluution luomat spesialisoituneet laitteet” siis olekaan Tooby & Cosmidesin ”keksintöä”, eikä edes amerikalaista alkuperää, vaan poliitinen ohjelma selsiten etsimiseksi on esitetty fas… ei kun europiireistä jo 1968, ennen kuin E. O. WILSONKAAN oli ”sosiobiologiaansa” esitellyt!

Kova on ollut paine ”keksiä jotakin”…  >:-]

http://www.ebbs-science.org/RULES.htm

“The object of the Society shall be the furtherance of scientific enquiry within the field of the ***interrelationships of brain mechanisms and behaviour*** …

>Yksi teoria peilisolujen syntymisestä on se että lapsena tapahtuvat käsien >tarrautumisliikkeet ja niiden visuaalinen havaitseminen muokkaavat osan >aivosoluista niin että ne pystyvät myöhemmin aiheuttamaan saman reaktion kun >toinenkin ihminen tekee vastaavan liikkeen .

Tuo on ehdollistumisteorian mukainen selitys eri aistinten informaation ja myös muiden toimia koskevien havaintojen yhdistämiselle. Ei TÄMÄ edelytä minkäänlaisia erikoisspesialisoituneita "pelisoluja".

>(tämä voisi ehkä selittää sen miksi ei-kädellisillä vastaavat kyvyt ovat heikommat, >peilisolujärjestelmä ei pääse kehittymään kovin hyväksi jos eläin ei pääse >seuraamaan omien ruumiinosiensa liikettä kasvojensa edessä jatkuvasti)

Höpölöpö. Tietysti peili on yksi apuväline muiden joukossa parantaa havaintokyky-ään, mutta kyllä se on ihmisellä hyvin uusi keksintö varrattuna muihin "etuihimme" apinoihin nähden...

>Toisaalta ei myöskään ole perusteltua vielä väittää, että peilisolujärjestelmän >kehityksessä ei myös geeneillä olisi osuutensa.

Kun sellaisia ei ole, niitä "peilisoluja", eivätkä nuo tutkimusmenetelmät edes mene solutasolle...

>Esim. pienet muutokset neuronien >signaloitinopeuksissa, haarakkeiden >pituuksissa, reagoimisessa välittäjäaineisiin ym. vaikuttavat ratkaisevasti >neuroplastisuuteen ja peilisolujen tapauksessa ehkä osaltaan autismin syntyyn.

Voivat vaikutta suoraan autismin syntyyn, jos niissä jossakin onjotakin hyvin poikkeuksellista,ei SIIHENKÄÄN tarvita erityisiä "peilisoluja"...

>Ihmisen peilisolujärjestelmä on huomattavan monimutkainen.

Grrr....

>Se aktivoituu selvästi määritellyssä >ajallisessa järjestyksessä noin 250 ms >kuluessa: näköaivokuori -> STS - >> päälaenlohkon alaosa -> Brocan alue - >> >liikeaivokuori. Brocan alue aktivoituu selvästi voimakkaammin liikeaivokuori. Brocan alue jäljittelyn aikana kuin sormen tai >suun liikkeiden suorittamisen >yhteydessä.

Ähhh... Brocan alueen aktivoituminen perustuu siihen perusfaktaan, että AJATTELU ON KIELELLISTÄ.

Venäläiset sitä aktivoitumista yrittivät kovasti silloisilla laitteilla näyttää toteen, mutta toiset, esimerkiksi behavioristit, eivät ottaneet uskoakseen näyttöön...

Mutta nyt uskovat,ja tietävät pilkulleen, mistä on kysymys, toisin kuin harit...

>On täysin mahdollista, että on olemassa geenejä joita ilman pelisolujärjestelmän >syntyminen ei olisi mahdollista.

Grrr...

>Ei tarvita kuin tiraus liikaa tai liian vähän dopamiinia tietyille aivoalueille ja tulevat >peilisolut opettelevatkin jonkun muun tehtävän.

Sitten ne EIVÄT OLE "OIKEITA PEILISOLUJA", vaan tavallisia ehdollisten refleksien hermostollisia solmualueita!

>Peilisolut ovat kiistatta neurotieteen merkittävin löytö pitkään aikaan.

Ne ovat samanlainen "merkittävä löytö" kuin Chomskyn "kielielin"...

>Nyt vain pitää oppia niiden toiminta, kehitys ja rakenne paljon paremmin.

Ei haaskata nyt rahaa hölynpölyteoriapohjalta lähtevään tutkimukseen, vaan tämä asia on pantava kansainväliseen syyniin, ja sitten pitää jatkaa niillä Lounasmaan hienoilla laitteilla tieteellisesti kestävältä teoriapohjalta.

RK

Muokannut: , 1/27/2013 2:13:36 PM


RK
14.09.2004 00:11:17
150677

Koko ja peilisolut...

Koko-gorillakin, jonka “älykkysosamääräksi on mainittu 90”, todistaa geenipeilisolujen puolesta:

http://nationalzoo.si.edu/publications/zoogoer/2002/4/primatethink.cfm

“ Frontal areas of the neocortex may also be involved in the use of visual information to plan and execute fine motor movements. When a monkey performs an action like reaching out and grasping a small object with its fingers, neurons in a certain part of the frontal neocortex “fire” wildly. Interestingly, Giacomo Rizzolatti from the University of Parma found that these same neurons fire when the monkey simply observes another monkey, or even a human, performing the same action. These mirror cells, as Rizzolatti dubbed them, may play a role in imitative behavior and learning through observation.

As the phrase “monkey see, monkey do” suggests,primates seem quite good at aping each other. In fact, striking examples of what appears to be observational learning come from studies of tool use in great apes. Primatologist Jane Goodall reported that infant and juvenile chimpanzees at Gombe National Park in Tanzania watch intently as their mothers break off small branches and poke them into holes, fishing for termites. The young chimps then make awkward attempts to copy their mothers. “


RK
14.09.2004 00:11:19
150679

Perustosiasiat: "peilisoluteoria" on "evoluutiopsykologiaa"

H5 kirjoitti 12.09.2004 (150560)...

>Hyvä RK

>Peilisolut ovat kiistatta neurotieteen merkttävin löytö pitkään aikaan. Nyt vain pitää >oppia niiden toiminta, kehitys ja rakenne paljon paremmin.

Näistä linkeitä ilmenee, että "peilisoluteoria" on kuin onkin tavaramerkin luojien Tooby & Cosmidesinkin tunnustamaa "evoluutiopsykologiaa" (ns. "kosmista tuubaa"):

http://www.cogweb.ucla.edu/ep/Conceptual-3.html

Täällä on se "asiayhteys", josta edellinen on poimittu.

http://www.cogweb.ucla.edu/ep/index.html

Ja täältä löytyy, mitä sitten se asiayhteys "todella on":

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/144845?page=2#144946

RK

Muokannut: , 1/27/2013 2:16:02 PM