#77. How the Cerebellum May Adjust the Gains of Reflexes [Neuroscience]

 

NE

Red, theory; black, fact

The cerebellum is a part of the brain involved in ensuring accuracy in the rate, range, and force of movements and is well known for its regular matrix-like structure and the many theories it has spawned. I myself spent years working on one such theory in a basement, without much to show for it. The present theory occurred to me decades later on the way home from a conference on brain-mind relationships at which many stimulating posters were presented.

Background about the cerebellum

The sensory inputs to the cerebellum are the mossy fibers, which drive the granule cells of the cerebellar cortex, whose axons are the parallel fibers. The spatial arrangement of the parallel fibers suggests a bundle of raw spaghetti or the bristles of a paint brush. These synapse on Purkinje cells at synapses that are probably plastic and thus capable of storing information. The Purkinje cells are the output cells of the cerebellar cortex. Thus, the synaptic inputs to these cells are a kind of watershed at which stimulus data becomes response data. The granule-cell axons are T-shaped: one arm of the T goes medial (toward the midplane of the body) and the other arm goes lateral (the opposite). Both arms are called parallel fibers. Parallel fibers are noteworthy for not being myelinated; the progress of nerve impulses through them is steady and not by jumps. The parallel fibers thus resemble a tapped delay line, and Desmond and Moore seem to have [paywall] proposed this in 1988.

The space-time graph of one granule-cell impulse entering the parallel-fiber array is thus V-shaped, and the omnibus graph is a lattice, or trellis, of intersecting Vs.

The cerebellar cortex is also innervated by climbing fibers, which are the axons of neurons in the inferior olive of the brainstem. These carry motion error signals and play a teacher role, teaching the Purkinje cells to avoid the error in future. Many error signals over time install specifications for physical performances in the cerebellar cortex. The inferior olivary neurons are all electrically connected by gap junctions, which allows rhythmic waves of excitation to roll through the entire structure. The climbing fibers only fire on the crests of these waves. Thus, the spacetime view of the cortical activity features climbing fiber impulses that cluster into diagonal bands. I am not sure what this adds up to, but what would be cute?

A space-time theory

Cute would be to have the climbing fiber diagonals parallel to half of the parallel-fiber diagonals and partly coinciding with the half with the same slope. Two distinct motor programs could therefore be stored in the same cortex depending on the direction of travel of the olivary waves. This makes sense, because each action you make has to be undone later, but not necessarily at the same speed or force. The same region of cortex might therefore store an action and it’s recovery.

The delay-line theory, revisited

As the parallel-fiber impulses roll along, they pass various Purkinje cells in order. If the response of a given Purkinje cell to the parallel-fiber action potential is either to fire or not fire one action potential, then the timing of delivery of inhibition to the deep cerebellar neurons could be controlled very precisely by the delay-line effect. (The Purkinje cells are inhibitory.) The output of the cerebellum comes from relatively small structures called the deep cerebellar nuclei, and there is a great convergence of Purkinje-cell axons on them, which are individually connected by powerful multiple synapses. If the inhibition serves to curtail a burst of action potentials triggered by a mossy-fiber collateral, then the number of action potentials in the burst could be accurately controlled. Therefore, the gain of a single-impulse reflex loop passing through the deep cerebellar nucleus could be accurately controlled. Accuracy in gains would plausibly be observed as accuracy in the rate, range, and force of movements, thus explaining how the cerebellum contributes to the control of movement. (Accuracy in the ranges of ballistic motions may depend on the accuracy of a ratio of gains in the reflexes ending in agonist vs. antagonist muscles.)

Control of the learning process

If a Purkinje cell fires too soon, the burst in the deep cerebellar nucleus neuron will be curtailed too soon, and the gain of the reflex loop will therefore be too low. The firing of the Purkinje cell will also disinhibit a spot in the inferior olive due to inhibitory feedback from the deep nucleus to the olive. I conjecture that if a movement error is subsequently detected somewhere in the brain, this results in a burst of synaptic release of some monoamine modulator into the inferior olive, which potentiates the firing of any recently-disinhibited olivary cell. On the next repetition of the faulty reflex, that olivary cell reliably fires, causing long-term depression of concurrently active parallel fiber synapses. Thus, the erroneous Purkinje cell firing is not repeated. However, if the firing of some other Purkinje cell hits the sweet spot, this success is detected somewhere in the brain and relayed via monoamine inputs to the cerebellar cortex where the signal potentiates the recently-active parallel-fiber synapse responsible, making the postsynaptic Purkinje cell more likely to fire in the same context in future. Purkinje cell firings that are too late are of lesser concern, because their effect on the deep nucleus neuron is censored by prior inhibition. Such post-optimum firings occurring early in learning will be mistaken for the optimum and thus consolidated, but these consolidations can be allowed to accumulate randomly until the optimum is hit.

Photo by Robina Weermeijer on Unsplash

#70. How Noncoding RNA May Work [chemistry]

 CH

Red, theory; black, fact.

Back, DNA; red, long noncoding RNA; green, transcription complex. I am assuming that transcription initiation involves a DNA-RNA triplex, but this is not essential to the theory. Imagine that a loop closes through an RNA running from bottom to top.

No junk DNA?

The junk-DNA concept is quite dead, killed by the finding that the noncoding sections (sections that do not specify functional proteins) have base-pair sequences that are highly conserved in evolution and are therefore doing something useful.

What does long non-coding RNA do?

This DNA is useful because the RNA transcripts made from it are useful, serving as controllers of the transcription process itself and thus, indirectly, of protein expression. (Changes in protein expression may be considered the immediate precursor of a cell's response to its environment, analogous to muscle contractions in an intact human.) Small noncoding RNAs seem to be repressors of transcription and long noncoding RNAs (lncRNA) may either repress or promote. (lncRNA molecules also control chromatin remodeling, but this may be an aspect of stem-cell differentiation during development.) Despite the accumulation of much biochemical information, summaries of what lncRNA seems to do for the cell have been vague, unfocussed, and unsatisfactory (to me).

Control of gene expression: background

The classical scheme of protein expression, due to Jacob and Monod, was discovered in bacteria, in which a signal molecule from the environment (lactose in the original discovery) acts by binding to a protein to change its conformation (folding pattern). The changed protein loses the ability to bind to DNA upstream from the sequence that specifies the lactase enzyme, where it normally acts to block transcription. The changed protein then desorbs from DNA, which triggers transcription of lactase messenger RNA, which is then translated into lactase enzyme, which confers on the bacterium the ability to digest lactose. Thus, the bacterium adapts to the availability of this food source.

Since I have a neuroscience degree, I naturally wonder if all this can be modelled in neurobiological terms. Clearly, it's a reflex, comparable to the spinal reflexes in vertebrates. An elementary sensorium goes in, and an elementary response comes out. But vertebrates also have something higher than spinal reflexes: operations by the brain. (Don't worry, I am not about to go off the deep end on you.)

My neuron-inspired theory of long non-coding RNA

I propose a coordinating role for the noncoding RNAs: rather than relying on a bunch of independently acting reflexes, eukaryotic cells can sense many promoter signals at once, as a gestalt, and respond with the expression of many proteins at once, as another gestalt. You do not need an entire brain to model this process, just one neuron. The synaptic inputs to the dendrites of the neuron can model the multiple promoter activations, and the eventual output of a nerve impulse (action potential) can represent the signal to co-express a certain set of proteins, which is hard-wired to that metaphorical neuron by axon collaterals. In real neurons, action potentials are generated by a positive feedback between membrane depolarization and activation of the voltage-gated sodium channel, which causes further depolarization, so around we go. This potential positive feedback can be translated into terms of molecular biology by supposing a cyclic, autocatalytic pattern of lncRNA transcription, in which each lncRNA transcript in the cycle activates the enhancer (which is like a promoter) of the DNA of the next lncRNA in the cycle. The neuron model suggests that the entire cycle has a low level of baseline activity (is "constitutively active" to some extent) but the inhibitory effect of the small noncoding RNAs (analogous to what is called the rheobase current in neurons) suppresses explosive activation. However, when substantially all the promoters in the cycle are activated simultaneously, such explosive transcription does occur. The messenger RNA of the proteins to be co-expressed as the coordinated response is generated as a co-product of lncRNA hyper-transcription, and the various DNA coding regions involved do not have to be on the same chromosome.

#68. Consciousness is Google Searches Within Your Brain [neuroscience]

NE

Red, theory; black, fact.

The Google search is one of those things that are too good a trick for Nature to miss (TGTNM) and she didn't, and it's called consciousness.

Brain mechanism of consciousness

I conjecture that the human brain launches something like a Google search each time an attentional focus develops. This is not necessarily a literal focus of activity on the cortex; it is almost certainly a sub-network activation. The sub-net activity relays through the prefrontal cortex and then back to sensory cortex, where it activates several more sub-nets; each of these, in turn, activates further sub-nets via the prefrontal relay, and so on, exponentially. At each stage, however, the degree of activation declines, thereby keeping the total cortical activation limited.

Accounting for subjective experience

The first-generation associations are likely to be high in the search rankings, and thus subjectively "close" to the triggering attentional focus and relatively strongly in consciousness, although still in the penumbra that is subjectively "around" the attentional focus. Lower-ranking search results would form a vast crowd of associations only dimly in consciousness, but would give conscious experience its richness. Occasionally, an association far out in the penumbra will be just what you are looking for, and will therefore be promoted to the next attentional focus: you get an idea.

The role of emotions

The evaluation process responsible for this may involve the mediolateral connections of the cortex, which lead back to the limbic system, where emotions are thought to be mediated, at the cingulate gyrus. Some kind of pattern recognition seems unavoidable, whereby a representation of what you desire <06-25-2021: itself a sub-network activation> elaborated by the mediolateral system is matched to retrieved associations. Your target may be only a part of the retrieved association, but will suffice to pull the association into the attentional focus.

This is a great system, because it allows a mammal to converge everything it knows on every task, rather than having to perform as a blinkered if-then machine.

Brain mechanisms and our evolutionary history

01-02-2021: Why should we have this back-and-forthing between the prefrontal cortex and the sensory association cortex? Two possibilities: 1) the backward projections serve a priming function, getting certain if-then rules closer to firing threshold in a context-sensitive manner; 2) This is a uniquely human adaptation for our ecological niche as environment modifiers. In ordinary tool use and manufacturing, dating back to Homo habilis, the built thing is smaller than the builder's body, but in environment modification, the built thing is larger than the builder's body—an important distinction. Thus, the builder can only see one part of it at a time. Viewings must therefore be interleaved with reorientations involving the eyes, neck, trunk, and feet. These reorientations, being motoric in nature, will be represented frontally, and I place these representations in the prefrontal cortex. The mental representation of the macro-built-thing therefore ends up being an interleaved collection of views and reorientations. <07-11-2021: In other words, a simulation.> The reorientations would have to be calibrated by the vestibular system to allow the various views to be assembled into a coherent whole. By this theory, consciousness is associated with environment modification.

05-24-2021: Consistent with this theory, the cortical representation of vestibular sense data is atypical. There is no "primary vestibular area." Rather, islands of vestibular-responsive neurons are scattered over the sensory cortex, distributing across the other senses. This seems analogous to a little annotation for xyz coordinates, etc., automatically inserted in a picture, as seen in computer-generated medical diagnostic images.

#66. Neuromodulators as Peril Specialists [Neuroscience]

NE

Red: theory; black, fact.

Solanum dulcamara, a plant with anticholinesterase activity.

“Life is Difficulty”

My PhD thesis was about a neuromodulator (acetylcholine) acting on mammalian brain. It was tough to decapitate all those rats; I never got used to it. But if you can’t stand the formaldehyde, get out of the lab.

The basic theory

I conjecture that the primordial function of any type of transmitter substance acting on the g-protein-coupled cell-surface receptors or nuclear receptors of neurons was to coordinate the whole-organism response to some class of perils.

 

Complications

Glutamate, GABA, and acetylcholine are usually considered neurotransmitters, not neuromodulators, but all three have G-protein-coupled receptors in addition to ionotropic receptors and are thus both.

In thermoregulation, hypothalamic glutamate and GABA act on the body via the serotonergic raphe pallidus nucleus. The implied connection with predation (See table) would be due to the fact that animals become torpid at extremes of temperature and thus easy prey. The larger predator would have a smaller surface to volume ratio and thus slower warming and cooling after leaving its refugium to hunt. The predator thermal advantage would have been the selection pressure for thermal sensitivity in the anti-predation system, which eventually became upstream of temperature regulation effectors generally. 

The functional assignments suggested in Table 1 would mostly pertain to a very primordial brain. The implication is that any modern biological function of the neuromodulator substance other than organizing the response to a specific type of peril was elaborated out of the primordial function over long-term evolution, which can act opportunistically to confer new functions on preexisting adaptations.

An example of such elaboration is shown for dopamine in the inferred social role. A pre-adaptation for this role split may have been breast-feeding.

Table 1.

Peril	Substance	Failure mode
Extremes of heat and cold	glutamate and GABA	?
Predator	serotonin	depression
Parasite	histamine	phobia
Rival conspecific	noradrenaline	paranoia
Social isolation

#49. The Reentrant-pathway Theory of Mental Illness [Neuroscience]

NE

Red, theory; black, fact.

This theory is a further development of post #45, “The Denervation supersensitivity Theory of Mental Illness.”

The basic idea here is that if a region of cerebral cortex is overgrown relative to a major synaptic partner, not only will it be starved of synaptic input from the partner, but it will also produce excess axons going to that partner that will have difficulty finding enough dendritic territories on which to synapse. Both difficulties can be solved at one stroke, however, if the overgrown area synapses on itself. The logic is similar to the application of valence rules in chemistry.

This mode of repair will produce cyclic signaling pathways (called “reentrant” in Neurospeak) that could support endlessly circulating neural activity. This is therefore an alternative way of getting what I have called “autonomous activity” from disregulated cortical growth, with no need to invoke the phenomenon of denervation supersensitivity. The loop circumnavigation time would have to be long enough to allow for the recovery of any refractory periods that may follow nerve-impulse firing.

The autonomous activity will give rise to hallucinations (called psychotic symptoms) if the re entrant pathway is in sensory cortex, and to manic behavior if in cortex with decidedly motoric functions, which would include planning. Since I have conjectured in these pages that an emotion is a high-level motor command, a re entrant pathway in frontal limbic cortex would produce an apparent emotion disconnected from conscious experience and if in posterior limbic cortex, a hallucinated emotion trigger.

The situation is very similar if a cortical area is normal in size but one of its main synaptic partners is reduced in size by disease. In epileptogenesis, the post-damage remodelling of the local neural networks is known to be associated with new-synapse formation and the sprouting of axon collaterals. The hyperexcitable brain tissue responsible for triggering seizures is known to lie just outside the dead core zone of the damaged region, and can therefore be called “overgrown” relative to the dead zone, which has zero functioning neurons.

All this is compatible with the formation, during the epileptogenesis latent period, of a pair of counter circulating, polysynaptic “ring roads” around the perimeter of the damaged area. This process would be determined by simple rules of valency satisfaction. Both ring roads would be capable of carrying autonomous activity that progresses to a seizure. This might only happen if inhibitory tone is also compromised. Hallucinations and seizures seem to be different grades of the same phenomenon.  Indeed, auditory hallucinations commonly occur in association with temporal-lobe seizures. The temporal lobe is the location of the auditory cortex (Brodmann areas 41 and 42).

#45. The Denervation-supersensitivity Theory of Mental Illness [neuroscience, evolution, genetics]

NE     EV     GE     

Red, theory; black, fact.

People get mental illness but animals seemingly do not, or at least not outside of artificial laboratory models such as the unpredictable, mild-stress rodent model of depression. A simple theory to account for this cites the paleontological fact that the human brain has been expanding at breakneck speed over recent evolutionary time and postulates that this expansion is ongoing at the present time, and that mental illness is the price we are paying for all this brain progress.

In other words, the mentally ill carry the unfavorable mutations that have to be selected out during this progress, and the mutation rate in certain categories of mutation affecting human brain development is elevated in modern humans by some sort of "adaptive" hot-spot system. "Adaptive" is in scare quotes here to indicate that the adaptation inheres in changes in the standard deviation of traits, not the average, and is therefore not Lamarkian.

In brain evolution, the growth changes in the various parts very probably have to be coordinated somehow. I conjecture that there is no master program doing this coordination. Rather, I conceive of the human brain as comprising scores of tissue "parcels," each with its own gene to control the final size that parcel reaches in development. (This idea is consistent with the finding of about 400 genes in humans that participate in establishing body size.) All harmonious symmetry, even left-right symmetry, would have to be painstakingly created by brute-force selection, involving the early deaths of millions of asymmetrical individuals. This idea was outlined in post 10.

Assuming that left and right sides must functionally cooperate to produce a fitness improvement, mutations affecting parcel growth must occur in linked, left-right pairs to avoid irreducible-complexity paradoxes. I have previously conjectured in these pages that the crossing-over phenomenon of egg and sperm maturation serves to create these linked pairs of mutations, where the two mutations are identified with the two ends of the DNA segment that translocates. (See "Can Irreducible Complexity Evolve?")

Most of the evolutionary expansion of the human brain appears to be focused on association cortex, which I conjecture implements if-then rules, like those making up the knowledge bases familiar from the field of artificial intelligence. The "if" part of the rule would be evaluated in post-Rolandic cortex, i.e., in temporal and parietal association cortices, and the "then" part of the rule would be created by the pre-Rolandic association cortex, i.e., the prefrontal cortex. The white matter tracts running forward in the brain would connect the "if" part with the "then" part, and the backward running white-matter tracts would carry priming signals to get other rules ready to "fire" if they are commonly used after the rule in question.

Due to such tight coordination, I would expect that the ideal brain will have a fixed ratio of prefrontal cortex to post-Rolandic association cortex. However, the random nature of the growth-gene bi-mutations (perhaps at mutational hot-spots) permitting human brain evolution will routinely violate this ideal ratio, leading to the creation of individuals having either too much prefrontal cortex or too much temporal/parietal cortex. In the former case, you will have prefrontal cortex starved of sensory input. In the latter case, you will have sensory association cortex starved of priming signals feeding back from motoric areas.

Denervation supersensitivity occurs when the normal nerve supply to a muscle is interrupted, resulting in a rapid overexpression of acetylcholine receptors on the muscle. This can be seen as an attempt to compensate for weak nerve transmission with a tremendous re-amplification of the signal by the muscle. Analogous effects have been found in areas of the cerebral cortex deprived of their normal supply of sensory signals, so the effect seems to be quite general.

In cases of genetically-determined frontal-parietal/temporal imbalance, I conjecture that the input-starved side develops something like denervation supersensitivity, making it prone to autonomous, noise-driven nervous activity.

If the growth excess is in sensory association cortex, this autonomous activity will manifest as hallucinations, resulting in a person with schizophrenia. If the growth excess is in the prefrontal cortex, however, the result of the autonomous activity will be mania or a phobia. Depression may originally have been an adaptation to the presence of a man-eating predator in the neighborhood, but in civilized contexts, it can get activated by the unpredictable (to the sufferer) punishments resulting from manic activity. If the mania is sufficiently mild to co-exist with depression, as in type II bipolar disorder, then the overall effect of the depressive component may be like a band-aid on the mania.

The non-overgrown association cortex might even secondarily develop the opposite of denervation supersensitivity as the result of continual bombardment with autonomous activity from the other side of the Rolandic fissure. This could account for the common observation of hypoprefrontality in cases of schizophrenia.

#42. Corporate Sin [evolutionary psychology]

EP

Red, theory; black, fact.

7-25-2018: A moment's reflection reveals that not all of humanly willed unhappiness is due to two persons interacting, either in a sadness cycle or an anger cycle. Wars of depopulation and wars of dispersal represent these interactions promoted to the level of entire societies. This promotion theory assumes that the same hard-wired wetware is being used for both levels, but with the addition of a few more bits of code to support the social level.

Theologians such as Bishop Baycroft, writing in "The Anglican Way," are well aware of this extra dimension of human misery, referring to it as "corporate sin," and admit that it is a more difficult problem than individual sin. The advice I give in "Signaletics for Salvation" (https://nightbull.blogspot.com) will not help you efficiently if your unhappiness has its roots in corporate sin (for example, if you are caught up in a military draft or are a slave), but it may be better than nothing. But let's see what we can surmise about those extra bits of code.

The basic design seems to be to transform a tiff between two individuals into a tiff between two leaders, then copy the emotions of the leaders into the heads of all the followers on both sides. Thus, a political leader is a kind of emotional conductor. This is why we have leaders.

By this theory, World War II was a tiff between Adolf Hitler and Winston Churchill, both famous for their speeches in which they inspired passions in their followers.

How do you get to be leader? The simplest answer seems to be that you just get famous and you are also someone who doesn't see a way to end his pain without involving the whole world. <07-21-22: As for how I ended my own pain, minding my own business and reaching out to family at times of need seems to have sufficed. I also had a talk with my federal MP at one point.>

An attractive theory about fame, in turn, is that all fame is 90% being-famous-for-being-famous, and 10% (or less) is being famous for something else, call it the predisposing factor. Human inter group interactions have the form we observe because these predisposing factors are not random but are due to natural selection. Furthermore, they are conditional upon prevailing conditions, such as the price of bread relative to wages. Finally, they already exist at the individual level. The process of garnering the absurd 90% of fame is the by-now familiar phenomenon of going viral, and its earlier historical equivalents. 

I imagine that this process is a positive feedback loop in the brain that involves the attentional system and Hebbian plasticity, the latter well known among students of neuroscience for having a built-in positive feedback. We also know that emotions are contagious (See: Hatfield E, Cacioppo JT, Rapson RL. Emotional Contagion. New York: Cambridge University Press, 1994).

The final bit of code we need to produce leaders and thus corporate sin is a tendency of this contagiousness to be potentiated by the famousness of the emoter one is observing. This mechanism of social control is distinctly different from the snowball effect that I likened to a black hole in an earlier post. It will take more thinking to decide which is more accurate.

#41. The Sadness Cycle [evolutionary psychology, neuroscience]

EP     NE     

Red, theory; black, fact.

7-20-2018: This post builds on "Signaletics for Salvation," a post in the companion blog, "Experimentalist's Progress, " at https://nightbull.blogspot.com. The theory part of that post is reprinted below with slight modification for the convenience of the reader.

The anger cycle and the sadness cycle reach their full flower in wars of dispersal and wars of depopulation, respectively. These were discussed in the post "Two Kinds of War" in this blog.

Wars of depopulation serve to prevent Malthusian disasters such as general famine. The sadness cycle is a form of altruism that facilitates this depopulation by making a portion of the population sad and suicidal and the remainder contemptuous and entitled. The contemptuous ones take everything the sad ones have, ultimately their lives, and the sad ones let them.

If the sacrificial lambs were fighting what is essentially a form of cannibalism tooth and nail, the transfer of property would leave the heritors with many injuries, which would defeat the purpose of the whole process, which is to leave the residual population stronger and healthier than before under conditions of restricted food supply. However, always bear in mind that the sad ones and the contemptuous ones are playing two roles within the same adaptation; if you can play one role, you can play the other. However, if you unfortunately carry some unfavorable mutation, you will be predisposed to the sad role. This is another way the adaptation leaves the population more robust than before.

Since no altruism can evolve in the presence of selfishness unless the altruists are only altruistic to other altruists, a signaling cycle is required to lock the altruists together to the exclusion of non-altruists. Thus, sadness induces contempt and contempt induces sadness, and so on in a vicious cycle leading to the complete destruction of the sad ones and the transfer of all their property specifically to the contemptuous ones. This dynamic could be the origin of elder abuse and clinical depression.

Macchiavelli wrote, "He is made contemptible who is held to be changeable, light, effeminate, pusillanimous, irresolute, and from these the Prince must guard himself as from a reef." The traits listed appear to be the symptoms of unacknowledged sadness, and were no doubt quite lethal in Macchiavelli's time. Due to the present skyrocketing of the world population with the concomitant "Calhoun effect" from crowding stress, we are no doubt due for a remacchiavellianization of daily life. For example, should I even be sharing these insights with you instead of keeping them to myself to my own advantage or at least posting them on a commercialized blog? Does my slowness to commercialize indicate suicidally self-giving tendencies that will one day prove fatal?

6-29-2018: The Anger Cycle (reprinted)

Much of human unhappiness comes from destructive, escalating signaling cycles, usually between two persons. Examples: arguments, feuds, schools of thought, gang wars, revolutions. The signals exchanged are initially personal expressions of anger. Importantly, these expressions are multi modal, and therefore highly redundant. (e.g., threatening utterances, tones of voice, facial expressions, gait, crashing and banging things, spying, following, etc.) Your anger comes out of you "through every pore."

These signals are too many and varied for conscious control, which is why most people remain enslaved by their signals and cycles. The anger cycle is presumed to escalate until one of the parties must leave the country. When people are threatened, they seek allies, so all of society eventually gets drawn in and polarized as the escalation proceeds apace, like a black hole. Therefore, it is a group that must eventually leave, not a single individual, which is the basis of the refugee phenomenon. 

In ecological terms, the refugee phenomenon is clearly sub serving the function of dispersal. However, dispersal-producing behavior is fundamentally altruistic in a backhanded way. The benefit to the supposed loser, the group that eventually gets driven out, is that occasionally they find a newly-emptied vacant habitat in which to settle and therefore can reproduce without competition. This is a tremendous benefit in evolutionary terms and may once have been great enough to redeem all the waste and suffering of human-style dispersal. 

However, altruistic behavior cannot evolve in the presence of non-altruists unless a signaling system is established to ensure that altruists are only altruistic to other altruists. That is why I lay so much emphasis on signaling here. The reason why the signals are so multi modal is that the altruism program probably breaks down occasionally because of the short-term advantages of being a non-altruist. This has probably happened many times in the past and the broken algorithm was repaired each time by natural selection with the addition of yet another signal component. 

Multi modality implies the existence of a neuronal OR-element somewhere on the sensory side, and the amygdalae could be these OR-elements. More precisely, the amygdalae could be specialized for providing OR-elements generally to the brain by virtue of a characteristic, unique amygdalar cytoarchitecture.

7-20-2018: The various signal cycles may reinforce each other. The four signal cycles that seem to form the framework of human life seem to have such an interdependence. These are: mother-child bonding, which could potentiate man-woman bonding, which could potentiate the anger cycle (via jealousy), which could potentiate the sadness cycle. These insights come from introspection and my own biographical data.

#40. The 1950 Ramp [population, genetics, evolutionary psychology, engineering, neuroscience]

PO     EN     EP     NE     GE     

Red, theory; black, fact.

6-01-2018; Since about 1950, the world population has been increasing along a remarkably steady ramp function with no slackening in the rate of increase yet apparent, although one cycle of oscillation in the slope occurred during the Sixties. Malthusian reasoning predicts an exponential increase, which this is not. From several lines of evidence, I keep coming back to the idea that humans must have a subconscious population controller in their heads, and yet such a controller would have leveled out the increase by now. Until now, no theory has sufficed to explain the facts.

I here propose that the natural population curve for humans in good times is a saw-tooth waveform, with population ramps alternating with political convulsions that result in a large group being expelled permanently, resulting in the precipitous but limited drop in local population density that ends the saw-tooth cycle. This cycle accomplishes the ecological dispersal function to which I allude many times in these pages. The population must ramp up for a time to sustainably create the numbers needed for the expulsions. The WHO population curve shows only a ramp because it is a worldwide figure and therefore population losses in expelling regions are balanced by population increases in welcoming regions. This also implies that human population has been increasing in a way unrestrained by food or resource availability or any other external constraint since 1950, to now.

Clearly, human population is being controlled by instinctive factors, but not to a constant absolute density, but rather to a constant rate of increase. Population density would go up along the much faster, steeper, and more disastrous exponential curve of Malthus if there were actually no controller.

My formal training in engineering and neuroscience justifies a bit of speculation as to mechanisms at this point. Look first for such a controller in the hypothalamus, already known to control other variables, such as temperature, by feedback principles.

In school, I was taught that nature does not reinvent the wheel, which I understand to mean that once a brain structure evolves to serve a particular computational function, it will be tapped for all future needs for such a calculation. This process may make it grow larger or develop sub-nuclei, but additional, independent nuclei for the same computation will never evolve.

I will continue to assume that the controller is a conventional PID controller, as in previous posts. To make it control rate of increase rather than absolute population density, you put a differentiator in the feedback pathway. Look first in the amygdala for such a differentiator. If you are of the opinion that human population control is urgent, then you must knock out this differentiator and replace it with a simple feed-through connection. Fortunately, one common way for evolution to implement differentiation in mammals is to begin with such a feed-through connection and supplement it with an inhibitory, slow, parallel feed-forward connection. If this is the case here, then you just inhibit the feed-forward pathway pharmacologically as specifically as may be, and the job is done. Subjectively, the effect of such a drug would be to take away people's ability to get used to higher population density in deciding how many children to have. An increased propensity to riot should not occur.

I assumed in the last post that the political convulsions that produce dispersal are triggered by the value on the integrator of the PID controller rising above a threshold. However, in the above design solution, the convulsion would be triggered by the raw, undifferentiated population-density signal rising above some threshold. Look in the amygdala for this signal as well. Consistent with this, bilateral removal of the amygdalae and hippocampi in monkeys is known to have a profound taming effect accompanied by hypersexuality, known as the Kluver-Bucy syndrome.

6-17-2018: To be consistent, I would have to say that the differentiator for the population signal is more likely to be in the hippocampal formation by the argument of nature not reinventing the wheel, because in an earlier post, I interpreted the hippocampus as the site of four successive differentiations that carry out a Fourier transform by mapping sinusiodal waves back onto themselves at a particular best frequency, in the presence of a map of such best frequencies.

However, this setup would require the creation of two neuron-to-neuron connections for its evolution; a first connection to send the amygdalar raw population signal to the hippocampus, and a second to send the differentiated result back for further processing. At best, this would require two simultaneous mutations. Either change by itself would be at best useless and could never be selected. This appears to be another example of irreducible complexity requiring the bi-mutation mechanism described in the previous post. 

The mechanisms usually offered to explain cases of apparent irreducible complexity, such as spandrelling, exaptation, and scaffolding, all appear to lack time efficiency and processiveness. I previously said that in evolution there are no (absolute)  deadlines, but relative deadlines can easily be created by an interaction of processes. In the presence of relative deadlines, such as adaptive footraces to be the first clade to exploit a newly-habitable area or a new niche, time is of the essence and selection for speed and evolvability can be expected. Such selection will create mechanisms such as crossing over that enhance evolvability.

#37. Two Kinds of War [evolutionary psychology, engineering, neuroscience]

EN     EP     NE     

Red, theory; black, fact.

3-17-2018: In my post "The Pilgrim and the Whale", I propose that much human conflict sub serves dispersal.

12-28-2017: There are probably two basic biological uses for human anger, the other one being an emergency brake on population increase that avoids Malthusian disasters by triggering wars. This kind of war ends life without being notably efficient in producing mass migration. This is the use discussed in my post "The Iatrogenic Conflicts of the Twentieth Century." Mention of the destruction of Coventry was struck out because it looks better suited to population reduction than to triggering mass migration.

3-12-2018: I have long wondered why the Four Horsemen of the Apocalypse seem to include two gentlemen both in charge of warlike matters. Why the apparent duplication? The above postscript may give the reason: one (the guy with the bow) represents wars of (absolute) depopulation and the other (the guy with the sword) represents wars of displacement (relative depopulation).

The Coventry Blitz did, however, produce so much mass migration into the countryside surrounding that city that it was an embarrassment for the British government, calling into question Britain’s willingness to fight. This got me thinking: was Coventry some kind of watershed, before which the conflict was of the displacement type, and afterward, of the depopulation type?

The facts bear this out, considering Nazi treatment of the Jews as a litmus test of the zeitgeist of that time. After coming to power in 1933, the Nazis aimed at forcing the Jews to emigrate, and by the outbreak of hostilities in September, 1939, 250,000 of Germany’s 437,000 Jews had done so. The Coventry Blitz was in November, 1940. The Holocaust began, in terms of men, women, and children all being targeted for execution, in August, 1941, nine months later. The German zeitgeist, and perhaps that of the world, seems to have shifted gears in the fall of 1940, aiming at depopulation rather than displacement. I am obviously assuming that the evolutionary, selectionist justification of the Holocaust given at the time, in forums such as the 1942 Wannsee conference, was a rationalization.

I conjecture that wars brought on by population pressure begin as the displacement type, and if this does not result in sufficient local reduction in population pressure after a certain time, the hostilities shift gears to the depopulation type of conflict. If human population is under PID [proportional-integral-differential] control by the subconscious, the event causing the shift could be the amount of signal accumulated on the integrator rising above some threshold. This may actually be a second threshold, with the first and lower threshold controlling the outbreak of a war of displacement.

A paradoxical outcome of Calhoun's overpopulation experiments on rodents can be explained in terms of such an integrator. By providing unlimited food and water to a founder population of rats or mice, with regular bedding changes and exclusion of predators and parasites, the rodents were allowed to increase their population to fabulous numbers. However, the rodents were given no extra space. As the population soared to incredible densities, all kinds of pathological behaviors appeared along with a great deal of violence. Birth rates plummeted after a "behavioral sink" developed, and remained low, never recovering, as the population decreased all the way to zero.

My interpretation of the behavioral sink is that it is integrator windup, a pathology of humanly engineered PID controllers, and possibly natural ones too. The signal accumulated on the integrator has been building for so long, and the population crash is so sudden, that not enough time is spent at population densities below set point to cancel the "control debt" on the integrator, so it continues to insanely command a zero birth rate even as the population is heading for zero.

George Santayana wrote that "Fanaticism consists of redoubling your efforts when you have forgotten your aim." [source, Wiki quotes, accessed 06-11-2018] Sounds like integrator windup to me.

3-17-2018: To clean up some loose ends, let us postulate a third and highest threshold of the control debt, which, if crossed, leads to the human behavioral sink and the possible destruction of the human race due to essentially psychological causes. In the behavioral sink, I postulate that everyone would be a ZPG fanatic and unable to change without pharmacological help. (Good old booze? May not be that simple.) 

I myself may be a "ZPG fanatic", and produced in exactly this way, because I was born in 1953, just before suburbia became important, and may represent what most people in this country would now be had suburbia not been invented to take down the population pressure. At only 2 months from retirement age, I continue to be a virgin with no plans to change my ways, and I may be a straw in the wind, a harbinger of worse to come.

11-26-2019: I can testify from my own experience that the human behavioral sink is more like passive-aggressive personality disorder than anything else, but with particular attention to punishing the opposite sex by ignoring them.

3-22-2018: Correction: the modern suburbs were invented in London 200 years ago, but underwent explosive growth in North America after WWII. By 1950, half the American population was suburban.

#28. The Origin of Consciousness [neuroscience]

NE

Red, theory; black, fact.

After perusing Gideon Rosenblatt's blog at the prompting of Google, I finally saw the need for this post.

I theorize that we begin life conscious only of our own emotions. Then the process of classical conditioning, first studied in animals, brings more and more of our environment into the circle of our consciousness, causing the contents of consciousness to become enriched in spatial and temporal detail. Thus, you are now able to be conscious of these words of mine on the screen. However, each stroke of each letter of each word of mine that now reaches your consciousness does so because, subjectively, it is "made of" pure emotion, and that emotion is yours.

Some analogies come to mind. Emotion as the molten tin that the typesetter pours into the mold, the casting process being classical conditioning and the copy the environmental data reported by our sense organs. Emotion as the bulk on one side of a fractal line and sensory data the bulk on the other side. Emotion as an intricately ramifying tree-like structure by which sensory details can send excitation down to the hypothalamus at the root and thus enter consciousness.

The status of "in consciousness" can in principle affect the cerebral cortex via the projections to cortex from the histaminergic tuberomamillary nucleus of the hypothalamus. Histamine is known to have an alerting effect on cortex, but to call it "alerting" may be to grossly undersell its significance. It may carry a consolidation signal  for declarative, episodic, and flash memory. Not for a second do I suppose all of that to be packed into the hippocampus, rather than being located in the only logical place for it: the vast expanse of the human cerebral cortex.

#24. The Pictures in Your Head [neuroscience]

NE

Red, theory; black, fact.

My post on the thalamus suggests that in thinking about the brain, we should maintain a sharp distinction between temporal information (signals most usefully plotted against time) and spatial information (signals most usefully plotted against space). Remember that the theory of General Relativity, which posits a unified space-time, applies only to energy and distance scales far from the quotidian.

In the thalamus post, I theorized about how the brain could tremendously data-compress temporal information using the Laplace transform, by which a continuous time function, classically containing an infinite number of points, can be re-represented as a mere handful of summarizing points called poles and zeroes, scattered on a two-dimensional plot called the complex frequency plane. Infinity down to a handful. Pretty good data compression, I'd say. The brain will tend to evolve data-compression schemes if these reduce the number of neurons needed for processing (I hereby assume that they always do), because neurons are metabolically expensive to maintain and evolution favors parsimony in the use of metabolic energy.

Ultimately, the efficiency of the Laplace transform seems to come from the fact that naturally-occurring time functions tend to be pretty stereotyped and repetitious: a branch nodding in the wind, leaves on it oscillating independently and more rapidly, the whole performance decaying exponentially to stillness with each calming of the wind; an iceberg calving discontinuously into the sea; astronomical cycles of perfect regularity; and a bacterial population growing exponentially, then shifting gears to a regime of ever-slowing growth as resources become limiting, the whole sequence following what is called a logistic curve.

Nature is very often described by differential equations, such as Maxwell's equations, those of General Relativity, and Schrodinger's Equation, the three greats. Other differential equations describe growth and decay processes, oscillations, diffusion, and passive but non-chemically energy-storing electrical and mechanical systems. A differential equation is one that contains at least one symbol representing the rate of change of a first variable versus a second variable. Moreover, differential equations seem to be relatively easy to derive from theories. The challenge is to solve the equation, not for a single number, but for a whole function that gives the actual value of the first variable versus the second variable, for purposes of making quantitative, testable predictions, thereby allowing testing of the theory itself. The Laplace transform greatly facilitates the solution of many of science's temporal differential equations, and these solutions are remarkably few and stereotyped: oscillations, growth/decay curves, and simple sums, magnifications, and/or products of these. Clearly, the complexity of the world comes not from its temporal information, but from it's spatial information. However, spatial regularities that might be exploited for spatial data compression are weaker than in the temporal case.

The main regularity in the spatial domain seems to be hierarchical clustering. For an example of this, let's return to the nodding branch. Petioles, veins, and teeth cluster to form a leaf. Leaves and twigs cluster to form a branch. Branches and trunk cluster to form a tree. Trees cluster to form a forest. This spatially clustered aspect of reality is being exploited currently in an approach to machine intelligence called "deep learning," where the successive stages in the hierarchy of the data are learned by successive hidden layers of simulated neurons in a neural net. Data is processed as it passes through the stack of layers, with successive layers learning to recognize successively larger clusters, representing these to the next layer as symbols simplified to aid further cluster recognition. This technology is based on discoveries about how the mammalian visual system operates. (For the seminal paper in the latter field, see Hubel and Wiesel, Journal of Physiology, 1959, 148[3], pp 574-591.)

Visual information passes successively through visual areas Brodmann 17, 18, and 19, with receptive fields becoming progressively larger and more complex, as would be expected from a hierarchical process of cluster recognition. The latter two areas, 18 and 19, are classed as association cortex, of which humans have the greatest amount of any primate. However, cluster recognition requires the use of neuron specialist sub-types, each looking for a very particular stimulus. To even cover most of the cluster-type possibilities, a large number of different specialists must be trained up. This does not seem like very good data compression from the standpoint of metabolic cost savings. Thus, the evolution of better ability with spatial information should require many more new neurons than with the case of temporal information.

My hypothesis here is that what is conferred by the comparatively large human cerebral cortex, especially the association cortices, is not general intelligence, but facility with using spatial information. We take it on and disgorge it like water-bombers. Think of a rock-climber sizing up a cliff face. Think of an architect, engineer, tool-and-die maker, or trades person reading a blueprint. Now look around you. Do we not have all these nice buildings to live and work in? Can any other animal claim as much? My hypothesis seems obvious when you look at it this way.

Mere possession of a well developed sense of vision will not necessarily confer such ability with spatial information. The eyes of a predatory bird, for instance, could simply be gathering mainly temporal information modulated onto light, and used as a servo error for dynamically homing in on prey. To make a difference, the spatial information has to have someplace to go when it reaches the higher brain. Conversely, our sense of hearing is far from useless in providing spatial information. We possess an elaborate network of brain-stem auditory centers for accomplishing exactly this. Clearly, the spatial/temporal issue is largely dissociable from the issue of sensory modality.

You may argue that the uniquely human power of language suggests that our cortical advantage is used for processing temporal information, because speech is a spaceless phenomenon that unfolds only in time. However, the leading theory of speech seems to be the Wittgenstein picture theory of meaning, which postulates that a statement shows its meaning by its logical structure. Bottom line: language as currently understood is entirely consistent with my hypothesis that humans are specialized for processing spatial information.

Since fossil and comparative evidence suggests that our large brain is our most recently evolved attribute, it is safe to suppose that it may be evolving still, for all we know. There may still be a huge existential premium on possession of improved spatial ability. For example, Napoleon's strategy for winning the decisive Battle of Austerlitz while badly outnumbered seems to have involved a lot of visualization. The cultural face of the zeitgeist may reflect this in shows and movies where the hero prevails as a result of superior use of spatial information. (e.g., Star Wars, Back to the Future, and many Warner Bros. cartoons). Many if not most of our competitive games take place on fields, courts, or boards, showing that they test the spatial abilities of the contestants. By now, the enterprising reader will be thinking, "All I have to do is emphasize the spatial [whatever that means], and I'll be a winner! What a great take-home!"

Let me know how it goes, because all this is just theory.

#23. Proxy Natural Selection: The God-shaped Gap at the Heart of Biology [genetics, evolution]

EV    GE    

Red, theory; black, fact.

2-06-2017

As promised, here is my detailed and hypothetical description of the entity responsible for compensating for the fact that our microbial, insect, and rodent competitors evolve much faster than we do because of their shorter generation times. In these pages, I have been variously calling this entity the intermind, the collective unconscious, the mover of the zeitgeist, and the real, investigable system that the word "God" points to. I here recant my former belief that epigenetic marks are likely to be the basis of an information storage system sufficient to support an independent evolution-like process. I will assume that the new system, "proxy natural selection" (PNS) is DNA-based.

11-20-2017

The acronym PNS is liable to be confused with "peripheral nervous system," so a better acronym would be "PGS," meaning "post-zygotic gamete selection."

2-06-2017

First, a refresher on how standard natural selection works. DNA undergoes point mutations (I will deal with the other main type of mutation later) that add diversity to the genome. The developmental process translates the various genotypes into a somewhat diverse set of phenotypes. Existential selection then ensues from the interaction of these phenotypes with the environment, made chronically stringent by population pressure. Differential reproduction of phenotypes then occurs, leading to changes in gene frequencies in the population gene pool. Such changes are the essence of evolution.

PNS assumes that the genome contains special if-then rules, perhaps implemented as cis-control-element/structural gene partnerships, that collectively simulate the presence of an objective function that dictates the desiderata of survival and replaces or stands in for existential selection. A given objective function is species-specific but has a generic resemblance across the species of a genus. The genus-averaged objective function evolves by species-replacement group selection, and can thus theoretically produce altruism between individuals. The if-then rules instruct the wiring of the hypothalamus during development, which thereby comes to dictate the organism's likes and dislikes in a way leading to species survival as well as (usually) individual survival. Routinely, however, some specific individuals end up sacrificed for the benefit of the species.

Here is how PNS may work. Crossing-over mutations during meiosis to produce sperm increase the diversity of the recombinotypes making up the sperm population. During subsequent fertilization and brain development, each recombinotype instructs a particular behavioral temperament, or idiosyncratotype. Temperament is assumed to be a set of if-then rules connecting certain experiences with the triggering of specific emotions. An emotion is a high-level, but in some ways stereotyped, motor command, the details of which are to be fleshed out during conscious planning before anything emerges as overt behavior. Each idiosyncratotype interacts with the environment and the result is proxy-evaluated by the hypothalamus to produce a proxy-fitness (p-fitness) measurement. The measurement is translated into blood-borne factors that travel from the brain to the gonads where they activate cell-surface receptors on the spermatogonia. Good p-fitness results in the recombination hot spots of the spermatogonia being stabilized, whereas poor p-fitness results in their further destabilization. 

Thus, good p-fitness leads to good penetrance of the paternal recombinotype into viable sperm, whereas poor p-fitness leads to poor penetrance, because of many further crossing-over events. Changes in hotspot activity could possibly be due to changes in cytosine methylation status. The result is within-lifetime changes in idiosyncratotype frequencies in the population, leading to changes in the gross behavior of the population in a way that favors species survival in the face of environmental fluctuations on an oligogenerational timescale. On such a timescale, neither standard natural selection nor synapse-based learning systems are serviceable.

2-07-2017

The female version of crossing over may set up a slow, random process of recombination that works in the background to gradually erase any improbable statistical distribution of recombinotypes that is not being actively maintained by PNS.

7-29-2017

Here is a better theory of female PNS. First, we need a definition. PNS focus: a function that is the target of most PNS. Thus, in trees, the PNS focus is bio elaboration of natural pesticides. In human males, the PNS focus is brain development and the broad outlines of emotional reactivity, and thus behavior. In human females, the PNS focus is the digestive process. The effectiveness of the latter could be evaluated while the female fetus is still in the womb, when the eggs are developing. The proxy fitness measure would be how well nourished the fetus is, which requires no sensory experience. This explains the developmental timing difference between oogenesis and spermatogenesis. Digestion would be fine tuned by the females for whatever types of food happen to be available in a given time and place.

8-18-2017

Experimental evidence for my proposed recombination mechanism of proxy natural selection has been available since 2011, as follows:

Stress-induced recombination and the mechanism of evolvability

by Weihao Zhong; Nicholas K. Priest

Behavioral Ecology and Sociobiology, 03/2011, Volume 65, Issue 3

permalink:

http://ncsu.summon.serialssolutions.com/#!/search?bookMark=ePnHCXMwfV1NS8QwEC2yBz9-gxL0JgTytUl7EUQU767nkDQJeCgu7uLv903SVlEQepx0pmky8yaTvJx3G-StuZsLiKLydSpLO8QEx8Ry3J3QgR9Nmx6t2tAivxGcaNhOFw9qZd-fdXcv9bQER26Kr0yMMsQJ6WK1mCHPZoBIbMp0QvbtMLH3wjKm9GfjtwbEen163D088_lSAT4i9js-xgi_DdSQBplcwQhXIQSggNjHVEpwUlIlK-uSyJI4JMRspZKKymyzTfqiu27vXVy3n__6wQO9GARIQVXsqyZEbt7TWDl-hNEj1wHg2A5EOiqbwBIM_b6xS_iVR7h2mxcNpTtPN7vf_NIcIq2HjEeotopifT_8L_XDwNsmtZR_V_2ECDxpxqOr6m9j_wpDiOrp_r6N82bqPhW0uWxt6i7PtYGRhgh9lP4C2uagLw

Abstract:

"The concept of evolvability is controversial. To some, it is simply a measure of the standing genetic variation in a population and can be captured by the narrow-sense heritability (h2). To others, evolvability refers to the capacity to generate heritable phenotypic variation. Many scientists, including Darwin, have argued that environmental variation can generate heritable phenotypic variation. However, their theories have been difficult to test.

 Recent theory on the evolution of sex and recombination provides a much simpler framework for evaluating evolvability. It shows that modifiers of recombination can increase in prevalence whenever low fitness individuals produce proportionately more recombinant offspring. Because recombination can generate heritable variation, stress-induced recombination might be a plausible mechanism of evolvability if populations exhibit a negative relationship between fitness and recombination. Here we use the fruit fly, Drosophila melanogaster, to test for this relationship.

We exposed females to mating stress, heat shock or cold shock and measured the temporary changes that occurred in reproductive output and the rate of chromosomal recombination. We found that each stress treatment increased the rate of recombination and that heat shock, but not mating stress or cold shock, generated a negative relationship between reproductive output and recombination rate. The negative relationship was absent in the low-stress controls, which suggests that fitness and recombination may only be associated under stressful conditions. Taken together, these findings suggest that stress-induced recombination might be a mechanism of evolvability."

However, my theory also has a macro aspect, namely that the definition of what constitutes "stress," in terms of neuron interconnections or chemical signaling pathways, itself  evolves, by species-replacement group selection. Support for that idea is the next thing I must search for in the literature. &&