Infants have a sense of probability

Probability of an event is measured as the number of ways in which the event can occur compared to the entire number of ways that constitute the event space (all events that can happen). thus, if a coin is tossed once then the probability of getting a head is 1 (no. of ways in which the head can occur) / 2 (the total number of events that can happen- either head or tail). Thus the probability is 0.5. This way of envisaging probability, as something which exits prior to the toss of coin, is important and should be distinguished form the statistical measure that also says that if you tossed the coin an infinite number of time you would get head on 50 % or half of the of trials. Thus, the statistical concept of probability of occurrence of an event and the intuitive concept based on event spaces are quite different.

It is no wonder that we are endowed with the statistical concept of measuring or predicting the likelihood of an event based on prior experiences and frequency of occurrences of the event. After all for us to survive this ability would be of much use, helping us predict future events based on past outcomes. however, whether a sense of probability based on event spaces is also likely to evolve was more doubtful. Now a recent study in PNAS by Teglas et al, suggests that infants have a sense of probability and that frequency-based judgments do not influence their predictions (or reaction times linked to expectation of the outcome) unless they are as old as 4 yrs of age. This strongly suggests that sense of probability has evolved and when the predictions based on that intuitive faculty are not inline with the frequency of actual past outcomes, then the frequency based reasoning only kicks in quite late in development. This is an important study as it somehow turns the table on frequency-based understanding of probability in humans as we intuitively fell.

Please find below excerpts from the same.

Rational agents should integrate probabilities in their predictions about uncertain future events. However, whether humans can do this, and if so, how this ability originates, are controversial issues. Here, we show that 12-month-olds have rational expectations about the future based on estimations of event possibilities, without the need of sampling past experiences. We also show that such natural expectations influence preschoolers’ reaction times, while frequencies modify motor responses, but not overt judgments, only after 4 years of age. Our results suggest that at the onset of human decision processes the mind contains an intuition of elementary probability that cannot be reduced to the encountered frequency of events or elementary heuristics.

Our experiments show that natural intuitions of probabilities guide expectations for future outcomes early in development. Infants put their early numerical knowledge of small quantities to the service of higher-level processes of event interpretation (20), shaping rational expectations of what comes next based on the probable outcomes of what they see now. Such intuitions do not arise by the proved human prowess at sampling distributions. When experienced frequency disagrees with prior probability, it is only after substantial exposure to a sample of outcomes that participants’ motor responses overcome natural expectations of the likely event, becoming slower for the likely but infrequent outcomes, and this only after 3 years. Indeed, even at 5, when the motor system adapts to experienced frequencies, the original probability intuitions still shape overt judgment.

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(One of) The gene for PPI discovered

Prepulse inhibition is an enduring phenotype of schizophrenia. In simple words, PPI is the diminished startle response exhibited by an organism, when a weaker stimulus precedes a stronger, normally-startle-response-producing stimulus. It is believed that PPI deficits result from the sensorimotor gating deficits present in Schizophrenia probands. the graphic below shows how the normal prepulse inhibition works. In schizophrenia, this doesn't quite work and the startle response does not diminish with a prepulse being present.


A recent study by Akiko et al in PLOS biology has found a gene that , when knocked out in mice, led to PPI deficits akin to that seen in Schizophrenia. They also used Quantitative Trait Loci method to find the gene associated with PPI and found FABP7 to fit the bill. I present here, the abstract, author's summary and conclusion.

Deficits in prepulse inhibition (PPI) are a biological marker for schizophrenia. To unravel the mechanisms that control PPI, we performed quantitative trait loci (QTL) analysis on 1,010 F2 mice derived by crossing C57BL/6 (B6) animals that show high PPI with C3H/He (C3) animals that show low PPI. We detected six major loci for PPI, six for the acoustic startle response, and four for latency to response peak, some of which were sex-dependent. A promising candidate on the Chromosome 10-QTL was Fabp7 (fatty acid binding protein 7, brain), a gene with functional links to the N-methyl-D-aspartic acid (NMDA) receptor and expression in astrocytes. Fabp7-deficient mice showed decreased PPI and a shortened startle response latency, typical of the QTL's proposed effects. A quantitative complementation test supported Fabp7 as a potential PPI-QTL gene, particularly in male mice. Disruption of Fabp7 attenuated neurogenesis in vivo. Human FABP7 showed altered expression in schizophrenic brains and genetic association with schizophrenia, which were both evident in males when samples were divided by sex. These results suggest that FABP7 plays a novel and crucial role, linking the NMDA, neurodevelopmental, and glial theories of schizophrenia pathology and the PPI endophenotype, with larger or overt effects in males. We also discuss the results from the perspective of fetal programming.

A startle response to an unexpected, strong startling stimulus can be suppressed by an immediately preceding low-intensity stimulus, thereby eliciting little behavioral response. This phenomenon, called prepulse inhibition (PPI), has been observed in all mammals tested and is thought to reflect sensory-motor gating functions in organisms. PPI is diminished in human schizophrenia, raising the possibility that PPI might serve as a potential biological marker for the disease. Once the genes regulating PPI in lower animals are identified, it is expected that the human orthologs will be strong candidate genes for schizophrenia. In this study, we first performed a genetic dissection of mouse PPI using quantitative trait loci analysis, which detects chromosomal regions harboring causative genes. Further analyses including those of knockout mice, allowed us to identify one potential causative gene, Fabp7 (fatty acid binding protein 7, brain), a chaperon for the essential fatty acid docosahexaenoic acid. Human studies showed that the FABP7 gene is modestly associated with schizophrenia and that transcript expression levels are up-regulated in schizophrenic brains. From these results, we propose that a FABP7 protein-mediated disturbance of essential lipid metabolism in developing brains may be one risk factor in the development of schizophrenia, with a greater effect in males.

The evidence accumulated in this study consistently supports causation by Fabp7 as the sole gene or one of the multiple genetic substrates underlying the Chromosome-10 QTL of PPI. The gene's effects may be exerted through differential regulation of transcript levels in B6 and C3 mice at a critical period. Importantly, the FABP7 gene, which is modestly associated with schizophrenia in the current study, has the potential to link together the three compelling etiological hypotheses of schizophrenia, namely the NMDA, developmental, and glial (astrocyte) theories . The gene appears to make a larger contribution to PPI and schizophrenia in males. The remaining newly identified but uncharacterized QTLs in this study should provide a valuable resource for continuing molecular studies into PPI and schizophrenia mechanisms. Finally, there are no established prophylactic interventions for schizophrenia. Our results raise the possibility of cohort studies to examine whether replenishment of DHA in pregnant mothers can be beneficial in reducing the chance of schizophrenia development in their offspring, especially for high-risk families. Such analyses should preferably take into account genotypes that affect function and expression of FABP7 via both direct and indirect mechanisms.

I am excited by this research. The endophenotype-leading-to-genotype sort of research is very promising in that it treats complex disorders like schizophrenia one small step at a time and by identifying genes that may be underlying the schizophrenic condition, give us insights into the mechanisms involved. Anyway, I myself strongly believe that sensory gating theory of schizophrenia is on the right track and studies like these can only lead us closer to solving the mystery. One particular thing to note is that FABP7 has differential sex effects with its effects being more prominent in males and this too fits nicely with the fact that schizophrenia is more common in males and occurs at earlier age.

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cortex maturation: lag, span and thickness: ADHD, Schizophrenia, autism , IQ

There is an article making waves regarding the delayed maturation of the cortex of children with ADHD and so I thought I will throw in my two cents and try to simplify things.

First what is cortex maturation- the cortex of normal children first increases in size (as presumably new connections are made) , reaches a peak around 8 years of age and then the cortex thins (as spurious connections are pruned). We normally think of more connections being more beneficial, so it stands to reason why pruning should happen- but more connections do not translate into better connections- we only need to retain the right connections - the spurious connections need to be mercilessly pruned, if we are to function correctly. A theory based on this logic also asserts that we are born synaesthetes, but the spurious connections get pruned under normal development.


Now there are several things that can go wrong with this wiring and pruning process. Too much wiring can leave you with a thicker than normal cortex , too much pruning can leave you with lesser connections than required for normal functioning. Also the achievement of normal thickness, and subsequent thinnness can be developmentally shifted or lag from the normal developmental plan. Finally the thickening and thinnening may be squeezed in time and may happen at a faster rate for some individuals. Conversely, this may be spread over a broader time period and o9ccur at a relatively slower rate for other individuals. Considering the three factors of Size ( peak thichkness/ thinnness achieved), Lag (start and end of thickening and thinning process) and Rate (faster development over small time frame or longer span with slow rate of pruning/ initial connection formation) one gets 6 combinations (if we treat them as independent of each other) . Also considering that Thickening (initial connection formation) and Thinning (subsequent pruning) may also be independent one gets 12 combinations. these are sufficiently complex for me to abstain from making any sweeping generalizations. So I'll go to data:
1. In ADHD, new research (as also highlighted above) reveals, that the development (thickening and thinning ) of cortex is similar to normal individuals- only it is slightly shifted and starts later. this explains why ADHD disappears after teenage and is a problem only in childhood.

2. Children with higher IQ have faster rate of thickening and thinning of cortex as seen from graphic below.

3. Research from Paul Thomsaon's lab at UCLA has shown that in schizophrenia the normal pruning process does not stop in teenage as in normal adults, but continues beyond the early teenage resulting in more pruning than is normal.
4. I've read claims that in Autism the cortex is thicker and that it matures early. I'm tempted to posit Autism as a reverse trend of schizophrenic maturation, but need more accurate refernces and would be highly obliged if someone points me to appropriate resources.


All this seems very promising and I would be watching ne23s related to these developments more closely in future , considering that some of these are comorbid - like autism and IQ in high functioning ASDers and Creativity and Schizophrenia.

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Schizophrenia: sensory gating and extracting meaning from noise

I have blogged extensively in the past regarding schizophrenia and how people that are on that end of the cognitive thinking style are marked by a propensity to abstract meaning from apparent noise and meaningless or coincidental events. This, I have contrasted with Autistic thinking style which does not endow meaning even where it is legitimate.

It is also well known that Schizophrenics have a deficit with sensory gating and thus have loose attention/ loose associations etc. and are generally marked by less focal attention. This may lead to lowered filtering of irrelevant stimuli, which may lead to unusual experiences.

It is my contention that these two aspects may be independent of each other and when they come together may lead to psychosis. The deficits in sensory gating give rise to unusual experiences, while the normal confabulating left-brain mechanisms would try to explain the unusual experiences or noise in terms of a coherent narrative. If the first propensity to endow more meaning to even meaningless stimuli gets conjuncted with sensory gating, one may strew together a narrative that is not in touch with reality and thus lead to full blown psychosis, including delusions and hallucinations.

A recent study has just demonstrated that Schizophrenics have a propensity to derive meaning out of what is auditory noise for other normal people. I think there are two issues involved here- first more words were extracted from the auditory noise signal by the schizophrenics, and second they gave meaning to those words by strewing them together as 'phrases'. The length of the phrases heard for prodormant schizophrenics, indicated whether they were likely to suffer from schizophrenia in the future, if not on medication. thus both sensory gating deficits and meaning-endowing deficits seem to be at work.

A tendency to extract messages from meaningless noise could be an early sign of schizophrenia, according to a study by Yale School of Medicine researchers.

The study this month in the British Journal of Psychiatry reported on 43 participants diagnosed with "prodromal symptoms"- meaning they exhibited early warning signs of psychosis such as social withdrawal, mild perceptual alterations, or misinterpretation of social cues.

Participants in the study were randomly assigned to take the anti-psychotic medication olanzapine or a placebo, and then symptoms and neuropsychological function were assessed for up to two years.

During the "babble task," participants listened with headphones to overlapping recordings of six speakers reading neutral texts, which made the words virtually incomprehensible. The participants were asked to repeat any words or phrases that they heard. Only four words-"increase," "children," "A-OK," and "Republican"-were consistently reproduced.

Eighty percent of the participants who "heard" phrases of four or more words in length went on to develop a schizophrenia-related illness during times that they were not taking olanzapine, said the lead author, Ralph Hoffman, M.D., associate professor of psychiatry. In contrast, only six percent of those in the study converted to schizophrenia-related illness if the phrases "heard" were less than three words in length.

"A tendency to extract message-like meaning from meaningless sensory information can, over time, produce a 'matrix of unreality' that triggers the initial psychotic phase of schizophrenia-spectrum disorders," Hoffman said.

To me, this is further support for my hypothesis that Schizophrenic thinking style is marked by extracting too much meaning and it also supports the popular attention-arousal model of schizophrenia that considers the sensory gating deficits leading to hyperarousal and that in turn leading to loose and defocussed attention and this feeding on itself in a downward spiral. you can learn more about the theory by watching this excellent video.

Note related, though relevant to schizophrenia, is a new study that finds that Schizophrenics are more 'theoretically ' rational as compared to normal people.

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Nature via Nurture: IQ via breastfeeding

The Nature vs Nurture debate is now old-fashioned and instead enlightened people like Malcom Gladwell have been reformulating it as Nature via Nurture where, for genes to make their impact, appropriate environmental agents have to be present. Ed Yong of the excellent Not Exactly rocket Science blog, blogs about a recent study that shows that IQ differences (of up to 7 points) in people with two different variants of a gene, FADS2, can be accomplished under the environmental conditions of breastfeeding. Thus, the gene, which is instrumental in metabolism of some fatty acids, leads to increase in IQ points, but only if the babies are breast-fed. The link seems that this gene is necessary to metabolize some of the the fatty acids present in mother's milk.

I especially like the implications for genetics, that Yong derives from this study.

The study also has big implications for gene-hunters. The usual tactic for finding genes linked to physical traits or behaviours is to scan the entire genome for genes that have direct and prominent effects.

But if the team had used this tactic, they would never have billed FADS2 as an IQ-related gene (I’m avoiding using the phrase “a gene for IQ” because it’s trite and misleading). That’s because there are no significant differences between the IQ scores of people with the two FADS2 variants if you take breastfeeding out of the equation. The upshot is that geneticists can look to the environment for important clues when looking for genes that affect human behaviour and health.

For the foreseeable future, it looks like the dichotomy of nature and nurture is dying. It’s proving to be far more interesting to look at how the two interact, and good examples are springing up fast.

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Terror Management, Death and Psychological Immune response

There is a new article in Time that reports on a new study that found that when people are confronted with existential anxiety provoked by thoughts of their imminent death, then instead of becoming sad, they paradoxically become happier, although the effect is subconscious.

Here's one for the annals of counterintuitive findings: When asked to contemplate the occasion of their own demise, people become happier than usual, instead of sadder, according to a new study in the November issue of Psychological Science. Researchers say it's a kind of psychological immune response — faced with thoughts of our own death, our brains automatically cope with the conscious feelings of distress by non consciously seeking out and triggering happy feelings, a mechanism that scientists theorize helps protect us from permanent depression or paralyzing despair.

It might explain the shift toward more positive emotions and thought processes as people age and approach death, and the preternaturally positive outlook that some terminally ill patients seem to muster.

There is a plenty of literature on Terror Management Theory that posits that when confronted with thoughts of our death (and the corresponding terror) we manage that terror by reaffirming our cultural identities and sense of self-esteem. The culture, and self esteem, presumably provides a meaning to our lives and as such are helpful in alleviating the terror of self death. The researcher, DeWall, was experimenting on TMT, when he came across this phenomenon, which has been dubbed as a psychological immune response. In the test, the affect , after mortality salience, was measured by having the students fill words that could either be filled as positive words or as neutral/ negative words. this is a good test of unconscious affect and they found that those exposed to mortality salience condition had unconscious positive affect.

About half of the students were asked to contemplate dying and being dead, and to write short essays describing what they imagined happening to them as they physically died. The other half of the group was asked to think and write about dental pain — decidedly unpleasant, but not quite as threatening. The researchers then set about evaluating the volunteers' emotions: First, the students were given standard psychological questionnaires designed to measure explicit affect and mood. Then they were given assessments of nonconscious mood: in word tests, volunteers were asked to complete fragments such as jo_ or ang_ _ with letters of their choice. Some word stems were intended to prompt either neutral or emotionally positive responses, such as jog or joy; others could be filled in neutrally or negatively — angle versus angry. In a separate word test, students paired a target word such as mouth with its best match: cheek, which is similar in meaning, or smile, which is similar in positive emotional content.

Another important finding the team found was that in depression, the psychological immune system is dysfunctional. thus, depressive people may go in a downward spiral as they contemplate their inevitable death or other social/ personal threats to their self-esteem etc.

In his current research, DeWall is finding that other threats, such as that of social rejection, elicit a similar psychological immune response — except, intriguingly, in depressed people — and he thinks that it's a mechanism that healthy people are probably employing constantly, as a way of fending off a lifetime of serious misfortunes: not just the looming specter of death, but also the fact that you're not going to get that promotion, or that your spouse is cheating on you, or that your kid is on drugs. "It's very difficult to keep people in bad moods, and I think this is one of the reasons why," says DeWall. "Let's say we didn't have this. I think we would have a lot more difficulty coping with failure and threats and our own mortality. It would be difficult for us to find solutions. We would be thinking about how bad we were feeling all the time."

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Consciousness continued: what vegetative patients can tell us about it.

A recent New Yorker article discusses patients in a vegetative or minimally conscious state and what the recent research about their consciousness status can inform us about consciousness in general. The article starts with the much publicized research of Owen's group that found that a woman, in a vegetative state, responded to verbal instructions and could imagine playing tennis. It also discusses what blindsight and neglect can tell us about (un)consciousness.

In the nineteen-eighties, researchers determined that patients who had the syndrome—now called “neglect”—could process some objects in the left field of vision. In one experiment, a patient was shown two pictures of a house. The images were identical except that, in one, flames were emerging from a window on the left side of the façade. The patient said that she couldn’t see any difference between the images, but, when she was asked which house she would want to occupy, she almost always chose the one that was not on fire. “This is more complex than blindsight, because it means that the patient was unconsciously able to interpret and understand the symbolic meaning of the pictures,” Naccache said. “It is a powerful experiment to demonstrate that unconscious perception and unconscious cognition can reach upper levels of the brain.”

The article then goes on to discuss Naccache's theories and here I can see parallels to both Greenfield's (sustained representation) and Koch's views (focus on content, an 'ignition' and networks).

“When we are conscious, the key property is our ability to report to ourselves or to others the content of the representation—as when I say, for example, ‘I am perceiving a flower,’ or the fact that I am conscious of speaking with you now on the telephone,” Naccache told me. “You have patients who are conscious, or who are able to make reports, but you can prove that some stimuli escaped their conscious reports, as in the case of blindsight or neglect. You can study the neural fate of these representations by showing that, even if the stimuli were not reported by the subject, they were still processed in the brain.”

Naccache believes that consciousness also requires an ability to sustain a representation over time, which Owen’s patient clearly was able to do. “In assessing apparently vegetative patients who are unable to speak, and thus report, the direction of research should be to look for sustained representation,” he said. “If we can prove by neuroimaging techniques that this person is able to actively maintain a given representation during tens of seconds, it provides strong evidence of conscious processing.”

Naccache has recently incorporated a third neurological feature into his definition of consciousness: broadcasting. In a person who is conscious, he explained, information entering the brain is processed in a few areas and then distributed—or broadcast—to many others. “It’s as though there is a kind of ignition in the brain, and then information is made available to a very rich number of regions,” Naccache told me. “And that makes sense, that the information is initially represented locally and then made available to a vast network, because the person has this ability to maintain the representation within the network for a long time.

The article also covers Giacino's work that supports more of Greenfields views with consciousness dependent on levels of arousal (which may map to the quantity of neuronal assemblies of Susan).

The woman had what Giacino calls a “drive disorder,” in which a patient is unable to speak, move, or, possibly, think unless physically stimulated—by touch. Doctors believe that such disorders are caused by damage to the limbic lobes or to other parts of the brain that trigger and sustain behavioral responses. Some patients with drive disorders respond to drugs that increase brain levels of dopamine, a neurotransmitter that is associated with arousal. “Imagine if the woman were in a nursing home,” Giacino said. “Somebody would stop by for three minutes, check her bedpan, and present simple commands like ‘Squeeze my hand,’ ‘Close your eyes,’ and ‘Open your mouth.’ She is not going to do any of those things, but she clearly had a significant amount of preserved function. It had to be harnessed externally.” At J.F.K. Johnson, patients with drive disorders receive behavioral and drug therapy. (Some patients improve, but prospects for recovery are largely determined by the extent and nature of the damage to the drive system.)

Giacino applied Deep brain stimulation to one such patient and got spectacular results.

The researchers speculated that, because of damage to the man’s frontal lobe, thalamus, and brain stem—areas involved in regulating arousal—the nerve signals in his brain were muted. As Nicholas Schiff, a neurologist at Weill Cornell Medical College who led the study of the man’s brain, put it, “It’s as if a radio were turned to such a low volume that you couldn’t hear the music distinctly.” He added, “The scans confirmed our expectation that this patient had a greater capacity for language than he demonstrated.”

The researchers described implanting electrodes in the man’s thalamus, which, by stimulating the brain tissue, had enabled him to regain considerable physical and mental function. “Deep brain stimulation can promote significant late functional recovery from severe traumatic brain injury,” they wrote. When the electrodes were turned on in the man’s thalamus, his speech improved, his movements became more fluid, and he was able to chew and swallow. When the researchers turned off the electrical stimulation, the man soon relapsed.

This is close to associating arousal with a minimum quantity to synchronous firing of neuronal assemblies; but what I most like is the ignition analogy of Naccache.

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The great consciousness debate

Over at the Mind blog, Deric has just posted a very fascinating exchange of opinions amongst Christof Koch and Susan Greenfield regarding the neural correlates of consciousness. the exchange seems to be from Scientific American, and in it both Christof and Susan put forward their views on the NCC and then have minor quibbles over particular conscious experiences / phenomenon. While Koch believes that consciousness of a percept arises from activation of a unique set of neurons, that form assemblies and networks and the neurons themselves differ from normal neurons (he implicates a strong role for layer 5 pyramidal neurons in Frontal cortex, having synapses with occipital visual areas, as being crucial for a conscious percept) , Susan insists that consciousness arises because of synchronous firing of neuronal assemblies - and the degree of consciousness depends on the number of neurons involved in that synchronous assembly (that lats up to millisecond intervals) . Thus while Koch focuses more on content of consciousness (and despite Susan's criticism that is an important area of investigation) and how it arises from a qualitative phenomenon (different types of neurons - pyramidal- involved), Susan focuses more on degrees of consciousness and takes consciousness to be a qualitative phenomenon. I, like Deric , find merit in both arguments.

Some excerpts:

Koch's view:

Physiologically, the likely substrate for NCC is a coalition of pyramidal neurons--a type of neuron that communicates over long ranges--within the cerebral cortex. Perhaps only a million such neurons--out of the 50 billion to 100 billion in our heads--are needed to form one of these coalitions. When, say, Susan enters a crowded room and I see her face, a coalition of neurons suddenly chatters in concert for a fraction of a second or longer. The coalition reaches from the back of the cortex, where representations of visual stimuli are first processed, into the front of the cortex, which carries out executive functions such as providing perspective and enabling planning. Such a coalition would be reinforced if I paid attention to the stimulus of her image on my retina, which would strengthen the amplitude or the synchrony of the activity among the select neurons. The coalition sustains itself and suppresses competing coalitions by feeding excitatory signals back and forth among the neurons in the back and front of the cortex. If, suddenly, someone calls my name, a different coalition of neurons in the auditory cortex arises. This coalition establishes two-way communication with the front of the brain and focuses my consciousness on the voice, suppressing the earlier coalition representing Susan's face, which fades from my awareness.

This notion about networks of neurons has received a boost from recent results by researchers at the Mount Sinai School of Medicine, Columbia University and the New York State Psychiatric Institute, working under Stuart C. Sealfon of Mount Sinai and Jay A. Gingrich of Columbia. Sealfon's and Gingrich's teams have demonstrated in genetically modified mice that hallucinogens--such as LSD, psilocybin (an ingredient of mushrooms) and mescaline--act on a type of molecule, called a serotonin receptor, found on the pyramidal cells that cluster in layer 5. The hypothesis that the mind-bending effects of hallucinogenic compounds come from activation of one receptor type on a specific set of neurons--rather than from "messing up" the brain's circuits in some holistic manner--can be further tested with molecular tools that can toggle layer 5 pyramidal cells on and off until the exact set of neurons being affected is identified.

Susan's views:

My own starting assumption is that there is no intrinsic, magical quality in any particular brain region or set of neurons that accounts for consciousness. We need to identify a special process within the brain. And to be a truly robust correlate of consciousness, this neuronal process must account for a variety of everyday phenomena, including the efficacy of an alarm clock, the action of anesthetics, the distinction of dreams from wakefulness, the existence of self-consciousness, the possible difference between human and animal consciousness, and the possible existence of fetal consciousness. A more plausible view of consciousness is that it is not generated by a qualitatively distinct property of the brain but by a quantitative increase in the holistic functioning of the brain. Consciousness grows as brains grow.

The central problem is that models developed by Llinas and others conceive of consciousness as an all-or-nothing condition. They fail to describe how the physical brain can accommodate the ebb and flow of a continuously variable conscious state. I favor an alternative. For more than a decade, scientists have known that the activity of tens of millions of neurons can synchronize for a few hundred milliseconds, then disband in less than a second. These "assemblies" of coordinating cells can vary continuously in just the right space and timescales for the here-and-now experience of consciousness. Wide-ranging networks of neurons assemble, disassemble and reassemble in coalitions that are unique to each moment. My model is that consciousness varies in degree from one moment to the next and that the number of neurons active within an assembly correlates with the degree of consciousness present at any given time.

This neuronal correlate of consciousness--the transient assembly--satisfies all the items on the shopping list of phenomena above. The efficacy of an alarm clock is explained as a very vigorous sensory input that triggers a large, synchronous assembly. Dreams and wakefulness differ because dreams result from a small assembly driven by weak internal stimuli, whereas wakefulness results from a larger assembly driven by stronger external stimuli. Anesthetics restrict the size of assemblies, thus inducing unconsciousness. Self-consciousness can arise only in a brain large and interconnected enough to devise extensive neuronal networks. The degree of consciousness in an animal or a human fetus depends on the sizes of their assemblies, too.

Take a look at the original debate as there is an even more more stimulating point-counterpoint section too.

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