Why Is Human Memory So Variable and Subjective?

I can mobilize an eidetic recall of the events at my last party in my apartment in New Orleans in May, 1969 (including the brew I was drinking), and yet a brother who visited me with a friend can't recall even being there. (I showed him the photos, and told him he was the one taking them.)  How is it I can recall this event including that he was there, in person, doing the photography, but he can't?

How is it that other events also may slip off the memory grid for him, and not for me, and in other cases slip off my memory grid but not his?  How is it my wife can exactly recall a movie we went to a year ago, but I can't? How is it I can recall exactly where my wife and I ate at Dallas-Ft. Worth airport in May, 2003 - while in transit to Barbados -but my wife can't?

All these questions and more occurred to me lately, and I began to inquire into why human memory is such a fragile, imperfect, subjective and variable thing. What we do know is that the hippocampus (named after its resemblance to the seahorse, from the Greek hippos meaning "horse" and kampos meaning "sea monster") plays important roles in the consolidation of information from short-term memory to long-term memory and spatial navigation. The hippocampus is located under the cerebral cortex . In primates it is located in the medial temporal lobe, underneath the cortical surface. It contains two main interlocking parts: Ammon's horn and and the dentate gyrus.

In Alzheimer's disease, the hippocampus is one of the first regions of the brain to suffer damage; memory loss and disorientation are included among the early symptoms. Damage to the hippocampus can also result from oxygen starvation (hypoxia), encephalitis, or medial temporal lobe epilepsy. People with extensive, bilateral hippocampal damage may experience anterograde amnesia—the inability to form or retain new memories.

In the case of Janice's cousin Desmond,  who died of Alzheimer's disease two years ago, the first memories lost were of distant events - while he retained memories of more recent ones. This is actually in contrast to how the disease usually presents, with long past events much more easily recalled than recent ones.


But let's leave out Alzheimer's and simply ask why memory varies so much in normal people, and how it is we differ so markedly in what events we can recall.  Some hints were presented in the Scientific American article 'The Language of the Brain' (October, 2012). What we learn is interesting to say the least.  This is in terms of "sequences of synchronized spikes"  in the particular cortical region to enable a critical factor in perception and memory.

As the article observes (p. 59):

"It appears that such synchrony acts to emphasize the importance of a particular perception or memory passing through conscious awareness."

In addition, evidently the degree to which we pay attention determines the frequency of the synchronized spikes in the 'gamma band' of frequencies (30 - 80 Hz).  The higher the frequency, the more numerous the synchronized spikes, the better a memory will be recalled. Further, gamma band signaling between distant cortical areas is also involved - as discovered by Pascal Fries of the Ernst Strugman Institute for Neuroscience.

Another interesting aspect of subjective memory I've found is that in places where I've actually lived over time I have much better memories of events than for the odd times I visit other locations - for relatively brief times. In the latter case, my memory is often patchy and unreliable. This is one reason whenever I travel now I keep a daily journal of events. In this way I can easily grab a journal kept over any past vacation, or brief interlude, and see what happened on such and such a day without having to play craps with my memory. (Which I admit is variable: excellent and eidetic in some realms and not so much in others!)

Research by Margarita Behrens of the Salk Institute - cited in the article - has also traced signal deficits to a neuronal cell called a "basket cell" - which is involved in synchronizing spikes in nearby circuits. An imbalance of either inhibition or excitation of these basket cells can then lead to reduced synchronized activity in the gamma band. Interestingly, this anomaly can also indicate neurological disorders such as autism and schizophrenia. These circuit anomalies may also be responsible for the thought disorders that often accompany schizophrenia.

We also learn (ibid.):

"When it comes to laying down memories, the relative timing of spikes seems to be as important as the rate of firing. In particular, the synchronized firing of spikes in the cortex is important for increasing the strengths of synapses- an important process in forming long term memories."

A synapse is "strengthened" whenever the firing of a neuron on one side of a synapse incites the neuron on the other side to register a stronger response. See e.g. the diagram below:

















How critical is this timing aspect? In 1997, researchers at the Max Planck Institute for Medical Research in Heidelberg, Germany,  found that a 20 milliseconds variance is all that's needed to throw a memory off. Thus, assuming a frequency in the gamma range, if an input at a synapse is consistently followed - within 10 milliseconds- by a spike from the neuron on the other side, then the memory is likely sealed. However, if the converse occurs, i.e. the neuron on the other side fires 10 milliseconds before the first one  all bets are off. The strength of the synapse between the cells decreases and the memory is then either fuzzy or lost.

The article ends by noting: that some of the strongest evidence that synchronized spikes may be important for memory comes from research by Gyorgy Buzsacki of New York University on the hippocampus. He found that the spiking of neurons in the hippocampus and other cortical regions it interacts with is strongly influenced by synchronous oscillations of brain waves in a range of frequencies from 4 to 8 hertz (the theta band). It seems that these theta band oscillations can coordinate the timing of spikes and have a "more permanent effect on the synapses."

This means the memory produced will be more long term, and better, more reliable.

In the end, memory is seen to be very dependent on synapse strengths and synchronization of specific types of waves (gamma and theta bands). If any one element is missing or off, then the memory simply can't be depended upon to yield accurate information - or maybe any information.

The moral of the story is that if we intend to trust our memories we better have those which resemble  the "memory masters" who possess the ability to recall what events happened on every day of their lives, e.g.
http://www.dailymail.co.uk/health/article-1340162/Memory-masters-The-people-rememberl-exactly-happened-day-lives.html

Failing that, we better learn to keep meticulous journals or take photographs of every major event we attend!

As for the key question: Why can't I remember that? The fault may not lie in one's 'stars' but in his synchronous spikes in the gamma band!

The Bid to Adjust and Manage the Atavistic Brain

The atavistic brain was discussed years ago by neuroscientist Michael Persinger, in his book,   The Neuropsychological Bases of God Beliefs.  Persinger's work was spurred to inception and completion by his notice of the regressive and atavistic component in many religiously inclined brains- especially those possessed by  avid fundamentalists.  He took care to distinguish this species, with their hellfire screeching and terrorist "witnessing" from the more laid back counterparts who, while they may have believed in the myth of personal Saviors and God-men, didn't try to foist it on others.

Persinger's work was motivated by a reality -based perception articulated in his biographical sketch in the same book:

"The research has been encouraged by the historical fact that most wars and group degradations are coupled implicitly to god beliefs and to the presumption that those who do not believe the same as the experient are somehow less human and hence expendable. Although these egocentric propensities may have had adaptive significance, their utility for the species' future may be questionable."


This was remarkable in clearly stating why judgmental religiosity was a toxic meme, and futher, had to be stomped out. His experiments, wherein he stimulated subjects' temporal lobes to excite religious epiphenomena (using a specially designed helmet) further disclosed that the primary site for the problems were located in the brain. If one could attack these brain regions properly, such as in the temporal lobes, it might even be possible to eradicate all excessive religious zealotry.

This take was not new, since in his interview with Persinger, Jack Hitt noted:

"Persinger is not the first to theorize that the Creator exists only in the complex landscape of the human noggin. In his controversial 1976 book, The Origin of Consciousness in the Breakdown of the Bicameral Mind, Julian Jaynes, a Princeton psychologist, argued that the brain activity of ancient people - those living roughly 3,500 years ago, prior to early evidence of consciousness such as logic, reason, and ethics - would have resembled that of modern schizophrenics"


Similarly, in a 1987 paper, (p. 137), Persinger boldly stated that:

"The God Experience is an artifact of transient changes in the temporal lobe”

Now, with the further development of quantum dot technology (see, e.g. 'The Quantum Dot: A Journey Into the Future of Microelectronics') we may well be on the cusp of controlling and regulating (at minimum) these atavistic brain tendencies which have produced everything from the Inquisition, to the Crusades, and even genocides. No human in his or her right mind could possibly dispute the fact that our species would be much better, operate more compassionately and perhaps even effectively in the social arena, if the brain could at least be subject to more regulation. At least the brains of those who need it.

The beauty of quantum dots is they can be specifically located in the exact brain regions where the most control is needed. If a feasible neural network mapping can be applied first, say to select input-output processing of hate and intolerance (as transmitted electro-chemical signals) in the brain's amygdala, is it not also possible to "disinfect" this tendency by altering the neural pathways and responses? Could the electro-chemical transfers effectively be cut off? Consider the most elemental input and output situation given by:


O o----------(e1)------(e2)------O (Z)


where e1 and e2 are two components by which an input at O yields a current (throughput)transferred to Z with information. The structure function of this would be: f(x1, x2) = x1*x2. But now suppose the component (e2) is negated or co-opted with another device. Then e2 = 0 and f(x1,x2) = 0. In other words the normal output one would expect is nullified.

We already know electro-chemical signals (via action potentials) are conveyed to  receptor neurons in the region of the amygdala. We note that when an axon is in its resting state it maintains a constant potential difference, or ‘resting membrane potential’ of –70 mV. When it is excited, it rises to a peak voltage of around 40 mV.  The latter basically arises from an uneven distribution of K+ (potassium) and Na+ (sodium) ions across the axon cell membrane relative to a collection of negatively charged protein molecules inside the cells.


Now, if neurons are stimulated – say by an electric shock from implants, an electronic monitoring device will show the 40 mV ‘action potentials’ on the traces. An interesting phenomenon associated with this, is that no matter the size of the stimulus applied, the action potential peak remains the same. What this shows is that even an appliance, device or artificial neural network (to "train the brain's receptors") placed in the immediate pathway will not stop the signal propagation. Like solar x-rays that can incept total communication blackouts, a way or mode must be found to short circuit the whole transfer process.


Note further that each pulse peak for the action potential coincides with a polarization change in the axon. Thus, as the pulse moves to a given site on the axon, Na+ ions move into the axon. Though technically both potassium and sodium ions are involved, there is actually a preferential bias. This bias is what we'll need to exploit in creating an adequate neural network to regulate the reception of impulses. This particular bias inheres in a preferential transferrence of Na+ ions through the axon membrane by a ratio that varies from 3:1 to 3:2 relative to K+ ions.

Thus, one way to engender a short circuit would be to alter the bias by altering the ion concentration at the axon membrane, say to 1:1. The synapses also have a role, of course, specifically the synaptic cleft. As I noted above, action potentials are constantly generated in an ‘all or nothing’ kind of way, and their endpoint is the synaptic cleft of the neuron. But here is where the ‘buck’ or rather the pulse, stops. Because as the axon has no choice in propagating the action potential, the neuron on the opposite side of the synapse (the post-synaptic cell) does have a choice of whether to fire or not fire when the potential arrives. If post synaptic neurons fired predictably with arrival of each and every action potential they’d be totally deterministic.


And boring. The fact that they need not fire, indicates a high degree of probability factored into the process. This process is depicted in Fig. 2 in simplified view, based on treating the axons as simple electrical ‘cables’ and the ends as ‘terminals’. This is perhaps the essential modus operandi for the brain acting as self-programmable von Neumann machine, particularly since quantum mechanics can easily be factored in.


In the diagram, we focus on Axon 1 and note that when the action potential arrives at the terminal it’s depolarized. This depolarization enables Calcium ions (Ca+2) already within the terminal to diffuse out into the mediating space. These ions follow a concentration gradient, unlike the case of the Na+ ions in the sodium pump. As the ions migrate, then diffuse to the post-synaptic cell (at Axon 2), they leave a channel in their wake that allows quantal releases of neurotransmitter (shown as a solid dot). These, like the Ca+2 ions diffuse across to the post-synaptic cell(s).


One neurotransmitter is acetylcholine. If the transmission of this or any similar chemical is rapid firing will occur, if not it won’t. Note also that Axon 2 must have a way of eliminating neurotransmitters almost as soon as they arrive. For acetylcholine, the enzyme cholinesterase acts to break it down into choline and acetate. In these inactive forms the neuron is spared being in a state of maximal and continuous excitation that would otherwise destroy it.


Generalizing the electrical cable analogy, the synapses act as switches in the system, the ‘on’ or ‘off’ positions denoted by information, in the form of chemical messages, to cross the synaptic cleft and trigger firing of the post-synaptic neuron(s) or not. Most probably there are bundles of similar neurons linked together by their respective connections, to perform critical functions. One might refer to the neuronal super-assembly or 'super-circuit’ within which considerations such as networks, and optimization of paths as well as 'adjacency and order' take precedence. Again, this is almost absurdly oversimplified since there really are no neurons that have only one connection to another. Indeed, we expect the typical neuron to have something like 10,000 connections to others.


But a start to how we might proceed is depicted  in the Kohonen SOM (Self-Organizing Map) in Fig. 3. Again, I reiterate, I'm keeping this at the most basic level. To reinforce this, trials performed quickly disclose Kohonen SOM  is too oversimplified. For example, it's applicable only to a single layer but the brain region under scrutiny is multi-layered. In addition, each "grid" neuron is an output neuron only. In real life, one must have both input and output neurons.Technically, we would need to examine and use the Multi-Layer Perceptron Network.

Anyway, as the Kohonen (SOM) is implemented, each input pattern gives rise to a localized region of activity in the feature map against a background of lower activity.For example, the activity may be registered as relative voltages, and these in turn may signify the ratio of Na+ ions to K+ ions. Once the Kohonen SOM is entrained, the aggregation of the input pattern should cause a localized group of neurons to be active.

However, the activity will almost surely not be what is desirable, because the simplicity of the map doesn't allow us to make drastic changes to the configuration of action potential thresholds.  In this case, using quantum dot implants - say for a fundie's brain - might well send him into convulsions, or worse. We certainly don't wish to have happen to the fundie what transpired with the main character in 'One Flew Over the Cuckoo's Nest' (i.e. after he was lobotomized at the end) we merely want to see his most reactive behavior tempered, so that he's tolerable, and more tolerant to others!

We ought to note here that already amazing steps have been made in terms of electronic implants, to control everything from over -eating to alcoholism. If these aberrant behaviors are within our purview, it is only a matter of time before excessive, meme (mind-virus) -driven zealous religiosity and its hate-driven actions derived from it are controlled.

See the following for information on the progress in electronic brain implants thus far:

http://www.wisegeek.com/what-is-a-brain-implant.htm#


http://www.electronicsweekly.com/blogs/david-manners-semiconductor-blog/2010/11/brain-implants-in-10-20-years.html


http://www.dailymail.co.uk/sciencetech/article-2087843/Living-cyborg-brains-created-laboratory--electrical-chips-replacing-missing-parts.html