Showing posts with label amygdala. Show all posts
Showing posts with label amygdala. Show all posts

Sunday, November 18, 2018

#44. Sunshine in Covey's Gap [evolutionary psychology, neuroscience]

EP     NE     
Red, theory; black, fact.

Who has not felt frustration at the difficulty and seeming impossibility of making a disagreeable emotion go away before we weaken and act it out, to our detriment? Techniques of true emotional control, i.e., making the bad feelings disappear rather than white-knuckle, open-ended resistance to acting them out, are not impossible, just non obvious. You just have to persuade yourself that this bad is good and believe it.

For the modern person, that second part, the believing, is difficult to achieve robustly if one is using religious solutions to the problem, the domain of soteriology (being "saved"), easier with psychoanalytical solutions, and, I am here to say, easiest of all with scientific solutions. "Believing," for me, means being prepared to bet your life on the truth of a proposition.

Steven Covey writes in "The Seven Habits of Highly Effective People" that between stimulus and [emotional] response, humans have, somewhat metaphorically, a "gap" in the causal chain and animals do not. In the gap, you find such things as imagination, self-awareness, conscience, and self will. He correctly lays tremendous emphasis on this point. George Santayana seems to have grasped this truth when he wrote: "Our dignity is not in what we do but in what we understand. The whole world is doing things." [source, Wiki quotes, accessed 11-06-2018]

Neuroscientist Joseph LeDoux has even elucidated what could be the neural pathways that make Covey's gap possible. A direct pathway from the thalamus to the amygdala mediates the basic fear response but an indirect pathway that leads from thalamus to cerebral cortex to amygdala provides a more nuanced, intelligent amendment to the first response. Full cancellation of the direct pathway by the indirect would account for Covey's gap, and in principle, this could be done by a cortical relay through the inhibitory interstitial neurons of the amygdala that terminate on the amygdalar projection cells.

The doctrines of classical religion probably lead to such cancellation of emotions such as hate and fear by activating the same circuits that are used by a parent to reassure a needlessly fearful infant.

Apparently, classical religion is all about getting people to do the right things for the wrong reasons. When the discipline of evolutionary psychology is sufficiently developed, we can look forward to the age when people do the right things for the right reasons.

Friday, July 20, 2018

#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.

Friday, June 1, 2018

#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.

Sunday, August 7, 2016

#12. The Neural Code, Part I: the Hippocampus [neuroscience, engineering]

EN    NE    
Red, theory; black, fact.

"Context information" is often invoked in neuroscience theory as an address for storing more specific data in memory, such as whatever climbing fibers carry into the cerebellar cortex (Marr theory), but what exactly is context, as a practical matter?

First, it must change on a much longer timescale than whatever it addresses. Second, it must also be accessible to a moving organism that follows habitual, repetitive pathways in patrolling its territory. Consideration of the mainstream theory that the hippocampus prepares a cognitive map of the organism's spatial environment suggests that context is a set of landmarks. It seems that a landmark will be any stimulus that appears repetitively. Since only rhythmically repeating functions have a classical discrete-frequency Fourier transform, the attempt to calculate such a transform could be considered a filter for extracting rhythmic signals from the sensory input. 

However, this is not enough for a landmark extractor because landmark signals are only repetitive, not rhythmic. Let us suppose, however, that variations in the intervals between arrivals at a given landmark are due entirely to programmed, adaptive variations in the overall tempo of the organism's behavior. A tempo increase will upscale all incoming frequencies by the same factor, and a tempo decrease will downscale them all by the same factor. Since these variations originate within the organism, the organism could send a "tempo efference copy" to the neuronal device that calculates the discrete Fourier transform, to slide the frequency axis left or right to compensate for tempo variations. 

Thus, the same landmark will always transform to the same set of activated spots in the frequency-amplitude-phase volume. I conjecture that the hippocampus calculates a discrete-frequency Fourier transform of all incoming sensory data, with lowest frequency represented ventrally and highest dorsally, and a with a linear temporal spectrum represented between. 

The negative feedback device that compensates tempo variations would be the loop through medial septum. The septum is the central hub of the network in which the EEG theta rhythm can be detected. This rhythm may be a central clock of unvarying frequency that serves as a reference for measuring tempo variations, possibly by a beat-frequency principle. 

The hippocampus could calculate the Fourier transform by exploiting the mathematical fact that a sinusoidal function differentiated four times in succession gives exactly the starting function, if its amplitude and frequency are both numerically equal to one. This could be done by the five-synapse loop from dentate gyrus to hippocampal CA3 to hippocampal CA1 to subiculum to entorhinal cortex, and back to dentate gyrus. The dentate gyrus looks anatomically unlike the others and may be the input site where amplitude standardization operations are performed, while the other four stages would be the actual differentiators. 

Differentiation would occur by the mechanism of a parallel shunt pathway through slowly-responding inhibitory interneurons, known to be present throughout the hippocampus. The other two spatial dimensions of the hippocampus would represent frequency and amplitude by setting up gradients in the gain of the differentiators. A given spot in the array maps the input function to itself only for one particular combination of frequency and transformed (i.e., output) amplitude. 

The self-mapping sets up a reverberation around the loop that makes the spot stand out functionally. All the concurrently active spots would constitute the context. This context could in principle reach the entire cerebral cortex via the fimbria fornix, mammillary bodies, and tuberomamillary nucleus of the hypothalamus, the latter being histaminergic.

The cortex may contain a novelty-detection function, source of the well-documented mismatch negativity found in oddball evoked-potential experiments. A stimulus found to be novel would go into a short term memory store in cortex. If a crisis develops while it is there, it is changed into a flash memory and wired up to the amygdala, which mediates visceral fear responses. In this way, a conditioned fear stimulus could be created. If a reward registers while the stimulus is in short term memory, it could be converted to a conditioned appetitive stimulus by a similar mechanism.

 I conjecture that all a person's declarative and episodic memories together are nothing more nor less than those that confer conditioned status on particular stimuli.

To become such a memory, a stimulus must first be found to be novel, and this is much less likely in the absence of a context signal; to put it another way, it is the combination of the context signal and the sensory stimulus that is found to be novel. Absent the context, and almost no simple stimulus will be novel. This may be the reason why at least one hippocampus must be functioning if declarative or episodic memories are to be formed.