Of Love, Friends and Animals

Continuing the trend set by Mixing Memory of starting the new year on a light and literary note, I would like to post a short story I had written way back in 1996, as an assignment in my creative writing class, and as a response to an assertion by my teacher that great literature usually involves good, complex and structured use of vocabulary and grammar. I was a rebel at that time and if she had made the opposing statement that simplicity is the essence of good literature would have come up with a radically different short story that would have had complex grammar and vocabulary:-)

PS: This story has relevance to the new year and is an imaginative account of trying to come up with a plausible scenario of why an unfortunate, real accident, as mentioned briefly and in passing in a newspaper report (The Times Of India dated 2/3 jan. 1996), took place.

__________*________*__________*__________

"Coming along?"

"Not today."

"Why?"

"Two reasons. I can do it better ..."

They laughed and understood.

"...and I'm going to meet her."

They couldn't pity him over this.

Jealous? Of course! They were his friends. He was leaving them for her.

"She doesn't love you"

"I love her"

The three word reply settled the matter.

"We won't go to the circus. We'll follow him."

They were his friends. They were young.
They could not be avoided.

__________*________*__________*__________

Long hours of waiting. Does time have a meaning? Hasn't this happened
before? Indeed, the 30th of Dec. comes every year. Which year are we
talking about? Does it matter? Not really!

And the place? Its familiar enough. Some inhabitants are wild. Some
docile. He soars towards the sky. She composes a symphony. He kills the
weak. She cheats and lies. Courage, Power, Deceit and Care. How are We
different from Them? They ought to call Us a Zoo. NO. We created
words. It is our right to call them Brutes. On second thoughts We are
different. We make Friends and We Love.


"Hello! Waiting for long?"
"I can wait for years."
A crane stood on one leg in the pool nearby.

She smiled. "Like all the other things?"
"Yes."

He could not find any hint of scorn in those words.
Love not only Blinds, It also Deafens.

She walked away. He followed.

They found themselves in front of the King.
Suddenly the world seemed to go into the reverse gear. They could feel
themselves in the cage. The tiger was moving around freely. Her eyes
rested on the beast admiringly.

She is not even looking in this direction.
How will she ever know?

But even when she was looking this way, She didn't notice
the garland.

She is clearly not in love. Then what Blinds her?
Bats are never found in zoos.



"I brought this garland for you."
Silence.


"I want to marry you."
A faint trace of smile. Derision, most probably.


"At our wedding I'll give you a star-studded garland. I'll
fight the gods for it."
The smile broadens. Contempt, definitely.


"I can do great things for you."
I don't know maybe but I feel I can.
"I can even kill this tiger."


Laughter. Pure, uninhibited laughter.


Screechhhhhh.chii.chii.grrr.grrrrr. A monkey jumped. As if to
synchronize, the tiger growled. The garland fell from his hands.

Scream. An involuntary, impulsive response. A natural reaction.


He was at heart a coward.
Every Man is.
Bravery is just an euphemism for foolhardiness.


Some people are different.
Her eyes flicked only briefly.
So what? That doesn't justify this. Why should she laugh at him?



"You'll marry me! You who kills the tiger and plucks the stars! Oh
coward! I am a tigress. If you have the courage to garland a tigress
then dare propose."


The garland was crushed as she walked over it.
So was his World.
And his self confidence.

Now he knew he couldn't. He was a coward.


"Oh coward!"
The words echoed from all directions. Some creations of his mind.
Others uttered by his friends.


They were his friends. They had followed him. Now they wanted to
destroy his boastful spirit once and for all.


"Oh coward!"
Those words were magical. His friends were making full use of
them.

__________*________*__________*__________

The friends spent the night together. They drank. He drank. More from
necessity than for pleasure.
They were happy and made plans for the New Year's Eve.


He wanted to drink more. They didn't allow him to. The wine cost a lot
and his share had been used up.
But things like that don't count in friendship.
They didn't want him to be sick.
That was the real reason.


He couldn't sleep. But was he awake? Hard to say. Definitely not
dreaming.


How could the sun ever rise again? And yet, somehow, morning dawned.

He remembered some money he had borrowed from them.
Moreover he returned it.
A new day had begun. He would have digested the liquor by now. So they
allowed him to drink more.
And he did. He drank it all.
Not only the liquor, but the taunts and the humiliation.

But there exist limits. He reached a stage when he could drink no more.

__________*________*__________*__________

Nobody, nothing obeys his commands now. Neither the tigers nor the
stars. Not even his own feet. They take him to places. Places he would
never want to go.

But wait. He is not alone .
What follows him is not his dishonor but one of his friends.

"Why am I standing here ? Is this tigress really brave? So am I."

His friend couldn't help laughing. He was also drunk. Out of pure
youth.
"Oh Coward ! If you have the courage to garland a tigress then
dare propose"
He mimicked. It was not only funny, it was also somehow
satisfying.

The object of his ridicule could not hear any words he said.
Yet the words were always the same.
He could hear them whether his ears were listening or not.

His eyes enjoyed greater freedom.
Tigress ... garland ... She ... friends.
Suddenly, the garland was in his hands.
Everything grew blurred except the tigress.

I am not a coward. Even if I am, I won't prove to be one.
I'll garland you honey, just like this tigress.

Security-men, wire-fence, moat, cage door. They'd lost their meaning.
Something else also lost its meaning and was turned into a ball of
torn flesh and blood.

__________*________*__________*__________

That night, New Year celebrations rocked the city.

She went to the party, unaware.
They drank and enjoyed themselves.

Their friend would not have liked them to ruin a New Year's night of
revelry. His being dead didn't mean that his will shouldn't be obeyed.
So they laughed and enjoyed themselves. They even saved some money from
their drinks to put an obituary next day. After all, they were his friends.

__________*________*__________*__________

Do let me know if you would like to read more of my stories. A happy new year to you all!!

Tags: literature, personal

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Depression and Stress: their bland tastes and their differential mediation and remeidal mechanisms vis a vis HRV and yoga

As per an interesting new research article, the Human
Taste thresholds are modulated by Serotonin and Norepinepherine. As per the Abstract:

Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease. In this study, we show for the first time that human taste thresholds are plastic and are lowered by modulation of systemic monoamines. Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%. In addition, the anxiety level was positively correlated with bitter and salt taste thresholds. We show that 5-HT and NA participate in setting taste thresholds, that human taste in normal healthy subjects is plastic, and that modulation of these neurotransmitters has distinct effects on different taste modalities. We present a model to explain these findings. In addition, we show that the general anxiety level is directly related to taste perception, suggesting that altered taste and appetite seen in affective disorders may reflect an actual change in the gustatory system.

What this means is that if you increase the amount of serotonin in the brain, then the capacity to detect sweet and bitter tastes is increased; if you increase noradrenaline levels those of detecting salty and bitter tastes is augmented; while a general increase in anxiety leads to better bitter taste detection. This also means that an anxiety state produces more bitter taste perception whereas a depressive state (characterized by low serotonin) is marked by bland sense of taste with marked inability to detect sweet and bitter tastes. A stressed state , marked by abundance of noradrenaline, would however lead to more salty and bitter taste perception.

It should be noted that different receptors and cells , in all taste regions of the tongue, for different human tastes have been found, and to me this seems evidence for five different flavors that have separate and distinct mechanisms and somehow model five different (chemical and taste) properties of the world.

Interesting to note that stress (which I loosely associate with noradrenaline) and depression which I loosely associate with serotonin) affect different taste receptors and thresholds. One can speculate that other major neurotransmitters like epinephrine (mediating stress and anxiety) may affect bitter taste; while GABA and dopamine may affect sour and ummami taste thresholds respectively.

Interesting again to note that generalized anxiety (most probably due to epinepherine levels) is tied to bitter taste and epinepherine acts on blood pressure, heart rate etc and so an epinepherine mediated response to stress could be via its effect on the Sympathetic Nervous System and affecting heart rate etc.

I would now like to rephrase the serotonin and norepinepherine distinction as that due to external lions haunting a zebra or internalized lions haunting an elephant and more generally in terms of Anxiety due to external stress and threat perception and Depression as a result of internalized stress and perceived threats. Please see discussion between me and Alvaro in comments on The Neugrogeneisis post for more perspective on this.

I'll like to move the discussion here towards an article Alvaro mentions in his commnets regarding Heart-Rate Variability (HRV) and how that measure is related to emotional regulation.


But before I do that, let me, before leaving the Taste senses, briefly highlight another Nature article in the same series, that mentions the retronasal system of olfaction and its relation to flavor perception. As per that article (you can read Mind Hacks comment on the same article here) , when we exhale, the retro nasal olfactory system kicks in, and by smelling the internal smells (of food being chewed for example), it leads us to perceive a flavor or taste that is actually based on an activation of a sense of smell and not taste proper. This is just so that the reader keeps in mind that senses of taste and smell are linked (by flavor) and it may be the case that a sense of smell may also be involved/ affected by emotional disorders like Anxiety and Depression.

What I propose is that Anxiety is a short term reaction to external stress; while depression is a long-term reaction to stress that is subsequently internalized. Thus, it is my contention that their mechanisms are different and their remedies too need to be different.

Alvaro, of Sharbrains, on the other hand contends that both are emotional dys-regulations and that HRV is a good indicator of how fit a person emotionally is and that teaching people how to regulate their emotions by providing them feedback about their HRV can be an effcetive tool against both. (Although, the sharp brains product FreezeFramre is focussed around Anxiety and external stressors and is intended for normal populations and not for depressed subjects; yet theoretically he seemed to believe that emotional regulation as indicated by a good HRV, should suffice to take care of both (Please correct me If I have interpreted wrongly, Alvaro). Also for some background on heart rate variability and its benefits go read the Sharpbrains entry in the 11th Encephalon hosted by me or more on this link.

Alvaro has pointed me to an excellent article and I agree broadly with him that emotional regulation and HRV should take care of both anxiety and depression. Yet the purpose of this post is to show that there must be (and are) subtle differences.

First for definitions (from the excellent paper Alvaro refereed to me).

The ANS, SNS and PNS:

A key system involved in the generation of this physiological arousal is the autonomic nervous system (ANS). The ANS is subdivided into an excitatory sympathetic nervous system (SNS) and an inhibitory parasympathetic nervous system (PNS) that often interact antagonistically to produce varying degrees of physiological arousal. During physical or psychological stress, activity of the SNS becomes dominant, producing physiological arousal to aid in adapting to the challenge. An increased pulse, or heart rate, is characteristic of this state of arousal. During periods of relative safety and stability, the PNS is dominant and maintains a lower degree of physiological arousal and a decreased heart rate. The ease with which an individual can transition between high and low arousal states is dependent on the ability of the ANS to rapidly vary heart rate.The PNS and SNS act antagonistically to influence cardiac activity.

For Heart Rate Variability (HRV):

Heart rate variability (HRV) is a measure of the continuous interplay between sympathetic and parasympathetic influences on heart rate that yields information about autonomic flexibility and thereby represents the capacity for regulated emotional responding. HRV reflects the degree to which cardiac activity can be modulated to meet changing situational demands.

This line caught my attention:

Although both autonomic branches exert a constant influence on heart rate, parasympathetic influence is predominant at rest and serves to maintain resting heart rate well below the intrinsic firing rate of the sinoatrial node.

I interpret this to mean that there is an intrinsic firing rate of sinoatrial node that is independent of PNS and SNS activities. This rate may be modfied by SNS to yield the resting heart rate, but there exists an independent compononent too to the heart rate.

Please note that there is a temporal difference in the action of PSN and ASN.

Sympathetic influence on heart rate is mediated by neurotransmission of norepinephrine and possesses a slow course of action on cardiac function. That is, changes in heart rate due to sympathetic activation unfold rather slowly, with peak effect observed after about 4 s and return to baseline after about 20 s. In contrast, parasympathetic regulation of the heart is mediated by acetylcholine neurotransmission and has a very short latency of response, with peak effect at about 0.5 s and return to baseline within 1 s.Owing to the difference in their latencies of action, the oscillations in heart rate produced by the two autonomic branches occur at different speeds, or frequencies.

Now the linkage with the nasal and smell systems:

Breathing air into the lungs temporarily gates off the influence of the parasympathetic influence on heart rate, producing a heart rate increase (see Berntson, Cacioppo, & Quigley, 1993). Breathing air out of the lungs reinstates parasympathetic influence on heart rate, resulting in a heart rate decrease. This rhythmic oscillation in heart rate produced by respiration is called respiratory sinus arrhythmia. As only cardiac parasympathetic activity possesses a latency of action rapid enough to covary with respiration, respiratory sinus arrhythmia is a phenomenon known to be entirely mediated by the PNS. In fact, a large majority of parasympathetically mediated variation in heart rate is produced by respiratory sinus arrhythmia.

I believe this connection between depression/ stress / taste/ retronasal olfactory systems/ smell/ nose/ yoga or paranayama/ breathing exercises to regulate HRV may be a valid linkage and the key behind breathing relaxation techniques for emotional regulation.


HRV is measured by various geometric and statistical means. We'll treat the simplest concept of HRV as implying the variance of heart beat rate (or interbeat interval) under different activities and spread over some interval to be a measure of HRV.

Statistical analyses are frequently reported and can be computed to represent overall HRV or HRV at different frequencies. For example, SDNN refers to the standard deviation of NN intervals, and SDANN refers to the standard deviation of the average NN interval computed across all 5-min recording segments.

Before discussing the hypothesized differences in HRV and emotional regulation in Depression Vs Anxiety/stress, I would like to briefly touch on one model of this HRV functionality that I find highly promising (it is a social and developmental model and takes into account evolutionary considerations).

Two major theories causally relate the autonomic flexibility represented by HRV with regulated emotional responding. Porges’s (1997, 2001) polyvagal theory is based within an evolutionary framework, which understands aspects of human functioning in terms of acquired, genetically based characteristics that are presumed to have aided in survival and/or reproduction throughout human phylogenetic history. Specifically, the polyvagal theory posits that the human ANS evolved in three stages, each characterized by the acquisition of an autonomic structure that plays a unique role in social processes. First acquired was the dorsal vagal complex, a slow-responding, unmyelinated vagus nerve that supports simple immobilization (e.g., freezing) in response to threat. This “vegetative vagus” slows heart rate through tonic inhibition of sinoatrial node activity. The capacity for active mobilization responses (e.g., fight or flight) became supported with the subsequent acquisition of the SNS. Most recently acquired was the ventral vagal complex, consisting of a fast-acting, myelinated vagus that can rapidly withdraw and reinstate its inhibitory influence on sinoatrial node activity.

The polyvagal theory states that the ability of the ventral vagal complex to rapidly withdraw its inhibitory influence allows humans to rapidly engage and disengage with their environment without the metabolic cost of activating the slower responding SNS. The dynamic nature of many social processes (e.g., nonverbal communication, romantic courtship) requires this rapid management of metabolic resources. Only when ventral vagal complex withdrawal is insufficient to meet demands are other autonomic subsystems enlisted. In this respect, the polyvagal theory emphasizes the relation of respiratory sinus arrhythmia (which purportedly indexes ventral vagal complex activity) and the regulation of the emotional processes underlying social behavior.

Finally lets look at some of the emperical research with HRV and emotional regulation disorders. There apperas to be robust data suggesting HRV is low or dysfunctional in anxiety disorders etc.

Coping refers to a set of regulatory strategies that are motivated by emotions (often negative emotions) and that frequently serve an emotion regulatory function but generally involve either nonemotional actions or nonemotional goals, or both (Gross, 1998). Higher levels of resting respiratory sinus arrhythmia have been associated with greater self-reported emotion regulation and the use of constructive coping strategies in university students (Fabes & Eisenberg,1997). This relation between resting respiratory sinus arrhythmia and constructive coping was mediated by negative emotional arousal.

Similarly, higher resting HRV was associated with reduced indices of distress in grade school children watching an upsetting film (Fabes,Eisenberg, & Eisenbud, 1993) and higher social competence in young children.

Recently bereaved individuals with higher resting respiratory sinus arrhythmia scored higher on measures of active coping and acceptance and lower on measures of passive coping. Female graduate students classified as repressive copers demonstrated lower resting LF and HF HRV near the time of a major examination than women classified as low anxious (Fuller, 1992), and women with lower parasympathetically mediated HRV (RMSSD) during experimentally induced fear states reported greater use of defensive coping (Pauls & Stemmler, 2003). Finally, those who exhibited submissive behavior during an interpersonal stressor had lower HRV (SDNN and RMSSD) at rest and during the task.

Now we come to Anxiety::

As predicted by the model, patients with generalized anxiety disorder have shown lower parasympathetically mediated HRV relative to controls during rest and during intense worry (Thayer, Friedman, & Borkovec, 1996). Lower overall and parasympathetically mediated HRV (aggregated across several tasks) have been observed in nonclinical panickers and blood phobics relative to controls (Friedman & Thayer, 1998a). Other manifestations of anxiety, such as trait anxiety (Fuller, 1992), social anxiety (Mezzacappa et al., 1997), and self-perceived stress induced anxiety (Sgoifo et al., 2003) have been associated with reduced resting parasympathetically mediated or overall HRV, suggesting the possibility that diminished autonomic flexibility may be an underlying causal factor.

It thus appears that in anxiety HRV is affected and is characterized by a simple low HRV value indicating lower emotional reactivity to external stress.

Now for depression (emphasis in article mine):

As with anxiety, it would be expected that diminished HRV would accompany depressive states given that a core feature of depression is the inability to generate appropriate positive and negative emotions . Consistent with this view, bereaved individuals and patients being treated for melancholic major depression with amitriptyline exhibited diminished resting parasympathetically mediated HRV, and patients with bibipolar depression showed reduced overall resting HRV . One study found decreased resting parasympathetically mediated HRV in depressed men, but increased HRV in depressed women . An inability to generate well-regulated autonomic responses to stress has been observed in depression, as those reporting greater depressive symptoms exhibited larger decreases from baseline in parasympathetically mediated HRV during a stressful speech task and smaller increases in parasympathetically mediated HRV during a cold pressor task , indicating a lessened capacity to regulate cardiac activity to meet the task demands. Resting overall and parasympathetically mediated HRV have interestingly been shown to increase with successful treatment of depression , suggesting that resting HRV is related to within-person variation in regulated emotional responding over time.

What I would like to emphasize is that depression is a second type of dis-regulation of Heart rate. While HRV captures the first rate variance that is ANS mediated, the baseline (or average) of heart rate variance may differ between people and within-a-person over time. In Manic episodes (when all the world is friendly and everyone an angel), the HRV may be very great; while in depressive episodes HRV may revert to a very low baseline level. It is my contention that this baseline Heart rate variability and the ability of heart to keep the HRV suited to task demands may be disrupted in depressive people as the baseline HRV has shifted. That is the depressive person will have a lower resting HRV than controls and given a control task would be unable to modify its HRV appropriately to meet task demand. To put matters simply while HRV measures the variance and flexibility in Heart rate and emotional regulation in response to an external event and low levels means inability to deal with external stress; The depression is characterized by low mean or baseline heart rate variability per se. This I suspect may be due to the lowered baseline firing rate of sinoarterial node an may have nothing to do with CNS, but might be directly influenced by CNS.

Hence my contention that we may need other tricks like CBT, RET for suitably modifying HRV and letting the HRV have a stable value over a long time period. Biofeedback, which would just indicate the variability with respect to current baseline , and would not reflect the cumulative history of the baseline Heart rates may not be helpful in treating depression thus.

Would love to hear other comments/ opinions.

Tags: depression, fitness, neuroscience, senses

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The Mouse is dreaming that it is in a Trap!!

New research has established that mice dream and during their sleep there is a two-way dialog between the hippocampal recent day memory area and the neo-cortex that is believed to be involved in long-term memory.


The content of the mice dream is also no longer secret. In the sleep they are replaying the sequence of steps that they had executed in a maze, but in a reverse order, and in lesser time and in general are rehearsing the structure of the maze (the mouse trap). Learning, it is to be remembered, arises from these replays of fast rewinds and sleep it seems is necessary for learning.

Some quotes from the article:

During nondreaming sleep, the neurons of both the hippocampus and the neocortex replayed memories — in repeated simultaneous bursts of electrical activity — of a task the rat learned the previous day.

Earlier this year Dr. Wilson reported that after running a maze, rats would replay their route during idle moments, as if to consolidate the memory, although the replay, surprisingly, was in reverse order of travel. These fast rewinds lasted a small fraction of the actual time spent on the journey.
In the findings reported today, the M.I.T. researchers say they detected the same replays occurring in the neocortex as well as in the hippocampus as the rats slept.

The rewinds appeared as components of repeated cycles of neural activity, each of which lasted just under a second. Because the cycles in the hippocampus and neocortex were synchronized, they seemed to be part of a dialogue between the two regions.

Because the fast rewinds in the neocortex tended to occur fractionally sooner than their counterparts in the hippocampus, the dialogue is probably being initiated by the neocortex, and reflects a querying of the hippocampus’s raw memory data, Dr. Wilson said.

“The neocortex is essentially asking the hippocampus to replay events that contain a certain image, place or sound,” he said. “The neocortex is trying to make sense of what is going on in the hippocampus and to build models of the world, to understand how and why things happen.”

PS: My blog post has deliberately used words like 'dream', 'mouse' and 'traps' instead of the correct 'sleep', 'rats' and 'mazes': just to come up with a juicy headline!!

Tags: , memory, learning, sleep

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Neurogeneisis, learning and small-world networks

Continuing this blog's recent focus on categorization, one possibility of how new items are classified has been hypothesized as either assimilitaion (adding the item to an existing schema in the feature space) or accomodation (addition of a new schema around the item in the feature space). We'll leave aside the newly introduced concept of Restructuring for this particular discussion.

Schemata, it is to be remembered, are conceptualized as nothing but a named cluster in the feature space. If we become a bit more audacious, we can posit that the clustering in the feature space is mimicked by the actual clustering/ connectivity of neurons in the Hippocampus (or the appropriate semantic memory brain module), with each neuron representing a particular item- say a neuron being a Halley Barry neuron. These neurons would not be randomly distributed- they form a small-world model with local clustering and bistability. whenever a group of neurons get activated together (and also belong to a cluster or clique), we can say that the memory of that category is activated.

Further suppose that learning and memory are crucially dependent on Neurogeneisis and new learning (of concepts ) happens by insertion of a new node (neuron in the small-world network of brain) and connecting it appropriately with other neurons.

As an example consider that all face recognition cells cluster together in the brain and the concept of face is activated by simultaneous activation of all cells of this cluster. The fact that a new visual stimulus (a novel human face of a stranger) is a face is determined by calculating the stimulus features and their difference from the prototypical/ exemplar face neurons and their features. A match so determined not only enables us to say that this new stimulus is a face (as this input would activate the face clique) , but would also give us an idea of where to place a new neuron that may encode for this new face and how to connect this with other neurons and with which other neurons.

Now whenever we encounter a novel stimulus we have two possibilities. If it matches some existing cluster / category, we encode this new memory by placing a new neuron coding for this in the region of that category in the feature space and (crucially) following preferential attachment attach it in a manner such that the probability of its linking to any other neighboring neuron is in proportion of the links that old neuron already has. (This can be readily implemented in brains as axonal connections will whither if not much functional activity happens at the synapse formed between the new neuron and the older one) . This is akin to assimilation of a new memory/ learning neuron. this method of insertion still keeps the neural net a small-world network.

Now consider the second case when the novel stimuli matches no older categories but necessitates that we form a new category if we have to represent that new item in the feature space. We need accommodation here. On the neural level this is still accomplished by inserting a new neuron, but this time the new node is not peripheral- the new neuron is a hub (category) neuron. So we use the method of copy to insert the new element. We copy the links (partially) of a neighboring hub (cluster center/ category label neuron) and use that link structure to link the newly introduced neuron in the small-world network. the network still remains scale-free and we have introduced a hub or a new category in this case.

All this seems very exciting. Some snippets from wikipedia article on scale -free networks are very relevant.

The mostly widely known generative model for a subset of scale-free networks is Barabási and Albert's (1999) rich get richer generative model in which each new Web page creates links to existent Web pages with a probability distribution which is not uniform, but proportional to the current in-degree of Web pages.

A different generative model is the copy model studied by Kumar et al. (2000), in which new nodes choose an existent node at random and copy a fraction of the links of the existent node. This also generates a power law.

Recently, Manev and Manev (Med. Hypotheses, 2005) proposed that small world networks may be operative in adult brain neurogenesis. Adult neurogenesis has been observed in mammalian brains, including those of humans, but a question remains: how do new neurons become functional in the adult brain? It is proposed that the random addition of only a few new neurons functions as a maintenance system for the brain's "small-world" networks. Randomly added to an orderly network, new links enhance signal propagation speed and synchronizability. Newly generated neurons are ideally suited to become such links: they are immature, form more new connections compared to mature ones, and their number but not their precise location may be maintained by continuous proliferation and dying off.

I am excited, what about you?

Tags: categorization, neuroscience, learning, memory

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Markers for Psychosis and Mania

A recent review of the COMT genotype Met/VAL SNP on psychiatric phenotypes of schizophrenia, bipolar mood disorder and schizoaffective disorder seems to suggest that the SNP's effcet mya be more of modifying the symptoms (with Val conferring positive symptom susceptibility and MET negative symptom susceptibility) of psychosis and mania, rather than conferring susceptibility to the diseases per se. Also the association, in European populations primarily, would be between both psychosis and mania (schizoaffcetive) present rather than juts a simple diagnosis of schizophrenia or bipolarity.

The narrowing of COMT linkages to the combination of Mania and Psychosis loks like a step forward and the distinction between symptom modifying effects and the distinction between symptoms based on their being positive (additions of functionality) or negative (deletion of functionality) seems to be a step in the right direction.

This differential effect of having a Met or Val allele on symptom type (positive and negative) is also inline with the inverted U model of dopamine levels that suggests that there is a range of dopamine levels that is good for the body(brain) and beyond either end there are deleterious effects. It could be that while a Met allele confers protective advantage for positive symptoms, it is an aggravator for negative symptoms. Depending on dopamine environmental levels, the person having Met allele may or may not show the symptoms of mania/ scizophrenia.

I am also intrigued by the BDNF met/val allele effect on anxiety susceptibility and forced to think whether there too the effect may be that of symptom modification rather than susceptibility?

Tags: depression, schizophrenia, genetics

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Categorization, Memory, small-world networks and neural architecture

In the last post I had wondered about the clustering based solution to categorization and how they may also inform us about how memory (semantic variety) is stored in brain, as semantic memory is best modeled by an associational or confectionist network.

Thus, a semantic memory based on clustering models may consist of associations between clusters or categories of information. For example one cluster may correspond to the names of countries and another to name of cities. A particular type of connection or association between these two clusters may map a relation of ----IS A CAPITAL OF ---- type where for example the fact that Paris is the capital of France is stored. For this knowledge to exist, one has to have prior notions of France is a Country and Paris is a City and on top of that an associational relation between the individual entities France and Paris belonging to particular clusters.

Much of this would be more apparent once relational models of categorization are also covered. For now let us assume that (semantic) memory itself may consist of clusters of neurons that are also interconnected. Interestingly one such neural architecture, that has also been able to simulate short-term memory has been the small-world network model. In this a large number of nodes (neurons ) are connected by edges (synapses) as in a typical random graph. These small-world networks are special in the sense that they have high clustering coefficients and low mean path length. Translated in English, this means they exhibit more than chance clustering (to enhance local processing) as well as display a small value of smallest mean path length (reflecting ease of global processing).


It is intriguing thta in the short term memory model using small-world networks simulation, the researchers found that the model could exhibit bistability, which may be crucial for memory formation. In bistability, the cluster or functional region corresponding to a particular memory can be in two states, depending on an input variable. Thus, a pulse (direction of attention) can activate/ deactivate a memory.

Crucially, it can be hypothesized that as the small-world network model of memory/ categorization is good for local-global processing as well as reflective of the actual brain and AI simulation architectures, the entire brain is a small-world network adequately categorizing and representing the sensory, motor and cognitive information and processing them.


A recent MEG based study has established the fact that the small-world network topology exists in functional sphere in the brain at all oscillatory levels (crucial for binding) and that seems very promising.

Tags: categorization, memory, AI

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Categoristation: how to bookmark the interesting pages on the web!

In an earlier post, I had touched upon the different categorization theories that are in prevalence. One of these that was discussed in details was the prototype Vs exemplar method that was based on clustering and involved different representational methods of the categories thus derived.

This post is about how a new item is allocated to a pre-existing category. Simplistically, and in the last post this was the position I had taken, it seems apparent that by calculating the distance of a new item in feature space from the central tendencies of the neighboring clusters (the prototypes/ exemplars) one can find a best fit with one of the clusters and allocate the new item to that category.

This is simplistic as it explains fitting of new items to existing categories, but does not include any mechanisms for formation of new categories.

The analogical approach I take here is of how do I decide in which folder to add a new bookmark of an interesting page found on the web. Most probably the names I have chose for my bookmarks folders are reflective of the central tendencies (common prominent features) of all pages bookmarked in that folder. I would normally look at the new page, and also at my existing folders and see if there is a best fit. If so I juts file the new bookmark under the best-fit existing folder. Slightly extending the concept of categorization to resemble that of a schema, this is the classical case of assimilation in a schema.

However, in case the new web-page cannot be filed under any existing bookmark folder, I would usually create a new folder (with an adequate descriptive name based on the location of the web page in the feature space) and file the new bookmark under that new folder. This is akin to trying to fit in a novel item into existing clusters in the feature space, only to discover, it doesnt fit well with any cluster, but is an outlier. The best way to accommodate such an outlier , in my opinion, is to create a new cluster around the outlier. Extending this to schema, it is not hard to see that this is the classical case of accommodation and formation of a new schemata to incorporate a novel item that cannot be assimilated in existing schema.

Piaget, of course , stopped here (and so do I, sometimes, when managing my bookmarks!). but I would like to venture firth and discuss the other process that I engage in , very infrequently, to keep my bookmarks in good shape. This is what I would call reorganization or restructuring. when I restructure my bookmarks, I change the names, I move bookmarks form one folder to another , I merge bookmarks and also at times create more than a few sub folders. Also, interestingly, I delete some of the old bookmarks; while am captivated by some of the bookmarks and even forget to complete the restructuring part.

I believe that we too indulge in restructuring of our Schema/ categories periodically (it may be as frequent as daily during REM sleep) and that a crucial form of learning is not juts Assimilation and Accommodation, but also Restructuring. Also it is my contention, that we consciously remember anything only because we have actively restructured that information and embedded it in a contextual narrative. In the absence of restructuring, there can be information that can be used, but no conscious knowledge.

I plan to tie this up with the 3 factor model of memory that is emerging. One factor of the memory system uses familiarity detection (assimilation), the other novelty detection(accommodation), while the other involves conscious and contextual recollection(restructuring).

I also propose that these three factors are behind the three kinds of memory (content-wise and not duration wise). The first type of memory is semantic (or noetic)- facts like France's capital is Paris; the second is procedural (or anoetic) - learning how to drive- and is unconscious; while the third is episodic or autonoetic) - personally remembered events and feelings) . Of course memories would also differer along the time dimension- working memory, long-term memory etc. , but that discussion is for another day.

Also a brief not to myself - how this may be linked with Hughling-Jackson's theory of 3 states of consciousness and how they are differentially affected in dissociation- the autonoetic memory would be affected first- the noetic second and the anoetic or unconscious memory last in dissociation.

Returning back to categorization, this approach of adding new items either by assimilation, accommodation or restructuring is more guided my Mind-Is-A-Container metaphor. Other metaphors of mind- assuming it theory like - may yield to new and interesting views of how we form a theory-like theory of categorization. The other minor variation to above mind is a container metaphor may be using labels for bookmarks (instead of folders)- this is what Google bookmarks and del.icio are using. I haven't experimented with that approach to bookmarking extensively, so am not sure what new insights can be gained form them. For those readers, who use labels to organize bookmarks, their insights as comments, would be greatly appreciated.

Tags: learning, memory, categorization

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Moral Intuitions: Musings continued.

In the last post, we dwelled on the classical trolley problem as well as a new type of moral dilemma that may be termed as the Airplane dilemma.

In some versions of the Airplane (as well as the Trolley ) problem, the problem is framed so as to implore us into examining our notions of trusting or being suspicious of strangers (terrorists scenarios) and to take into account the past as well as future characteristics of these people (like high IQ and national celebrity status) to arrive at a moral decision, as to serving whom would be a more moral action for the doctor. The airplane problem mostly focuses on Trust Vs Suspiciousness dimension, is people-centered and focuses on assessing people and situations correctly in a limited amount of time. After the decision is made, then the action is more or less straight-forward.

The trolley problem is also similar, but of a somewhat different nature. Here, the focus is on actions and outcomes. The Morality of action is judged by its outcome as well as other factors like whether the (in) action was due to negligence, indirect, personalty motivated etc. The people centered focus is limited to using-as-means versus ends-in-themselves distinction and in the later problems (president-in-the-yard) that of guilty vs innocent. The innocent, careful child playing on unused track, while the careless , ignorant five idiots playing on the used track is another variation that plays on this careful action versus careless action distinction.

It is my contention that while the Trolley problem aptly makes clear the various distinction and subtleties involved in an Action predicate, viz whether the action is intentional, whether it is accidental- and if so how much negligence is involved; whether (in)action could be prevented/ executed differently for different outcomes etc; it does not offer much insight on how to evaluate Outcome Predicate or the Intention Predicates.

In the Trolley Problem, while the intentional vs accidental difference may guide our intuition regarding good and evil , in case of positive or negative outcomes; the careful versus careless (negligent) action guides our intuitions regarding the normal day-to-day good and bad acts. Here a distinction must be made between Evil (intentionally bad outcome) versus Bad acts(accidental or negligent bad outcome).One can even make a distinction between Good acts (performed with good intentions) versus Lucky acts (accidental good outcomes, maybe due to fortuitous care exhibited). Thus, a child playing on an unused track may juts be a 'bad' child; but five guilty men tied on tracks (even by a mad philosopher) are an 'evil' lot. Our intuitions, thus , would be different in the two cases and would not necessarily be determined by utilitarian concerns like number of lives.

Some formulations of the airplane problem, on the other hand , relate to quick assessment of people and situations and whether to trust or be suspicious. The problem is complicated by the fact that should the doctor invest time in gathering more data/ confirming/rejecting her suspicion versus acting quickly and potentially aggravating the situation/ long-term outcome. These formulations and our intuitive answers may tell us more about the intention predicates we normally use. Whether we intend to be trusting, innocent and trustworthy or suspicious, cautious and careful. If cautious and careful, how much assessment/ fact gathering we must first resort to to arrive at the correct decision, before committing to single-minded and careful action.
Should we juts look at the past for arriving at a decision, or should we also predict the future and take that into account? If we do predict the Outcomes, then the Consequence predicate is long-term or short-term? Is it an optimistic or a worst-case outcome scenario?

There are no easy answers. But neither is the grammar of any language supposed to be easy. Constructing valid and moral sentences as per a universal moral grammar should be an equally developmentally demanding task.

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