Contents:  

1. Fundamentals of Neurobiology

2. Spinal Cord and Reticular Formation

3. Oculomotor System

4. Cerebellum

5. Cerebral Cortex and Basal Ganglion

6. Complex Memory and Thought

Fundamentals of Neurobiology  

            Many genes contain introns, pieces of DNA code that, when the gene is converted to RNA have to be spliced out in order for protein synthesis from the RNA to begin.  When an intron is spliced out it acts as a key for any gene that contains the code to produce the same intron.  For any RNA splicer there will almost always be an analogous DNA splicer somewhere in nature.  Consequentially, sooner or later an individual will be exposed to such a molecule and will thereby have that intron within them transferred to a number of other genes.  When the body tries to express a gene that’s had an intron copied in this way it generates an RNA and hence the intron.  As one of the other genes that possesses the same intron produces an RNA, this intron RNA can be fitted into the forming RNA strand as a prefabricated component, thereby increasing the rate of production.  In this way, the production of one protein becomes tied to the production of others so that increasing production of one increases production of the others.  Moreover, if the intron for one gene is located near the end of the code while the intron for another is at the beginning then the effect of an intron will be different.  At the beginning of the code the intron will be involved in whether the RNA will be produced at all, while at the end, an intron can only speed up RNA production.  So, when a random exposure to a DNA splicer is experienced, a cell’s or organism’s protein production will be changed, with genes activating simultaneously and/or in cascades and the relative amounts of produced proteins being set.  By natural selection beneficial locations for these introns are favoured and detrimental locations are eliminated.

            Long introns of this sort will have a great effect on which genes express themselves together.  Short introns will effect protein production to a lesser extent since they fill in a much smaller portion on the encoding RNA so that most of the RNA must be formed from individual RNA nucleotides.  However, sensory proteins can exist, possibly but not necessarily in the cell membrane, that bind such small RNA introns until a precise chemical interacts with them.  At such a time, the sensory protein releases its intron, the intron then inducing genes to increase production.  The introns that result from these activations can then potentially induce cascades of other genes to activate, thereby creating a complex, evolved reaction to an outside stimulus.  When the chemical is absent the sensory proteins bind to their particular introns and thereby, by removing all of those particular introns, inhibit gene expression.  By including the sensory protein or proteins for a particular chemical among the genes that are activated by it, exposure to a chemical can result not only in a response to the chemical, but also to an increased sensitivity to the chemical as more sensory proteins are produced.  In this way, a cell can focus its attention on those molecules that are in its environment and not waste protein production on making itself sensitive to molecules that are absent.  Further, sensory proteins that are within the cell can be sensitive to metabolic molecules (food molecules) and can thereby control protein production to ensure that there are enough, and not to many, proteins within the cell to perform its metabolic functions.

            The majority of chemical reactions are reversible.  It just happens that a large number of reactions within the body are one way as a result of energy molecules (ATP, ect.) which use energy acquired from food molecules to exert chemical force on those reactions to go in one direction.   An intron splicer that doesn’t use an energy molecule will operate in both directions, splicing introns out of messenger RNAs, but also splicing them back into messenger RNAs.  However, nothing says which introns will be spliced back, so almost any available intron can end up being spliced into a given messenger RNA.  This splicing in of introns that didn’t originally come with the RNA doesn’t normally change the proteins produced since messenger RNAs are not usually converted to proteins until all introns are removed.  A significant exception to this is anti-body production.

            When foreign organisms enter the body they survive by eating or otherwise interacting with the chemicals within the body.  Organisms that do not do this will eventually starve within the body so long as the body is fairly good at cleaning out chemicals that it doesn’t use.  Since these organisms are able to interact with the chemicals in the body, most of which are proteins, the body can use this interaction to effect them.  By producing antibodies that contain the protein the foreign organism is trying to interact with, the attempt by such organisms to take advantage of this protein can be inhibited.  The antibodies act by binding to and blocking the operation of the proteins on, or that have been released by the organism that tries to interact with a particular protein in the body.  For most proteins in the body there are other proteins that interact with them, for instance, those allowing for communication between cells.  When antibodies are formed to deal with foreign interactions with a protein they cannot differentiate between foreign and internal proteins.  As a result, these antibodies can interfere with or disable the operation of a protein within the body.  If such a protein is vital to an individual’s survival or health in the short run, the result can be injury or death, not by the organism but by the immune response to the organism.  Therefore, temporarily shutting down the antibody immune system is valuable in the treatment of serious or fatal viral and bacterial diseases.  There are two other purposes for antibodies.  The presence of a disease organism will produce a great deal of a particular detrimental protein, but the body is always producing its own proteins.  By producing a small amount of antibodies continuously, the body can rid itself of excess proteins that it accumulates over time.  In this way, it keeps the amount of potential food for disease organisms to a minimum and thereby makes it difficult for diseases to gain a foothold.  Secondly, by removing messenger proteins the body ensures that these proteins cannot travel far from their origins.  This ensures that the majority of chemical signals that reach a particular cell are from the same or nearby tissues, which, for instance, allows the body to use protein messengers for cells to identify their locations in the body.

            In order to make antibodies a cell must be able to bind a general antibody protein to any one of its other proteins.  Since a cell can splice any intron within its genes into numerous other locations, if any intron within the cell encodes for an antibody protein, this intron can be spliced into any gene that that cell is expressing.  Alternatively, if this intron encodes for a piece of protein that an antibody protein can bind to, then it could modify proteins to automatically bind with any free, general antibody proteins.  Either way, a random protein from the individual’s genome is bound to an antibody protein that will inhibit the function of anything that that random protein binds to.  Now, it appears that not all cells in to body put out antibodies.  In order to create antibodies a cell must allow RNAs with introns to be converted to proteins and secondly, the genes that contain the antibody introns must be active, must be producing RNAs so that the antibody introns are available for splicing.  By controlling which cells behave in these ways the body can control which cells it chooses to devote to antibody production.  Since the expression of genes effects the role of a cell in the body, a single antibody cell cannot produce every possible antibody and still remain an antibody cell.  In order to be specialized, the proteins that make this cell an antibody cell must dominate, and yet an antibody cell must put out large amounts of antibodies to deal with every protein the body makes.  By making a particular cell express only a few random proteins beyond those that produce antibody cells, these proteins can be prevented from having the effects they would have when combined with the other proteins that make a particular tissue that particular tissue.  Besides the antibody introns there is likely another functional intron, an intron that binds itself into the cell membrane and detects when the protein it’s connected to interacts with something else.  In this way, when there is an abundance of a protein that the antibody cell’s antibodies interact with, the cell can change its behaviour to react to this situations.  By increasing the production of proteins from the DNA the cell will increase the production of its antibodies and thereby act to suppress the target protein’s abundancy.  In addition to this, increased protein production will increase the rate of reproduction of the cells and thereby increase the number of antibody cells that produce that particular antibody.  An increase in the antibody cells will make the individual more sensitive to the foreign protein and hence create greater resistance to the disease that produced it.  Alone, this would result in the individual becoming allergic to any protein that interacts with the proteins of their body after their first exposure to it.  Each time they were exposed to the protein after the first, would cause their body to react as though it was exposed to a disease organism.  In order to prevent this reaction the antibody cells have to be sensitive to the activities of the rest of the immune system.  When the lysing cells (cells that break apart the cell membranes of foreign cells that enter the body) are actively responding to a disease, they send out a messenger protein to tell the body, including the antibody cells, that a disease organism is present.  If the antibody cells detect this messenger protein then, if they detect a protein that their antibodies would interact with, it is reasonably likely that a disease is producing that protein.  So, it is desirable for it to produce large amounts of its antibodies and reproduce in order to suppress the disease.  If the cell doesn’t detect the messenger protein then there is probably no disease to respond to and therefore the foreign protein will likely pass through the body quickly enough on its own.  If the messenger protein is detected, but no protein that interacts with that particular cell’s antibodies, then that particular antibody cell cannot act against the disease and therefore should remain inactive. 

One of the primary causes of allergies is when the lysing cells continually put out their messenger protein in reaction to a foreign single celled organism that they are somehow unable to destroy, and as a result, any interacting protein that enters the body is treated as through it’s coming from that organism.  Another cause of allergies is when an individual antibody cell mutates so that it always responds as though a disease organism is present.   Once this happens, any exposure to an interacting protein will cause that particular antibody cell to reproduce over all others of its type, thereby causing it to rapidly become the dominant antibody cell for that particular antibody.  A lack of exposure to the proteins their antibodies interact with will cause the population of a particular antibody cell to diminish since these cells require such proteins to induce them to reproduce.  Since an abundance of antibody cells acts to greatly diminish the interacting proteins through the activity of their antibodies, a sensitivity, either through disease or allergy, will cause a relatively rapid reduction in population of antibody cells.  Consequentially, disease organisms that remain in the body after the disease is suppressed will give the person a permanent resistance to that disease be maintaining the population of antibody cells that counter it, but diseases that are completely obliterated by the immune system will result in a lose of resistance.  To maintain resistance to such diseases the individual must be frequently exposed to the disease while their body is still resistant so that the interacting proteins of that disease will be able to induce reproduction of antibody cells.  It’s when an individual is completely isolated from one of these diseases, and hence loses resistance entirely, that the disease is able to get out of control enough to produce symptoms.

            Intron splicers can also splice free introns into RNAs that have many suitable locations into which to splice such introns.  Within the cells that produce proteins from intron containing RNAs this operation is of little use since the proteins created will generally be random and non-functional.  Rather, this operation of splicing numerous introns into one RNA (whether this RNA produces proteins or not is not significant) allows for a basis for memory.  In order to remember something you need to take all of the stimuli around you and bind them together so that they can all be released at a future time.  Since many of the introns are attached to sensory proteins, when the cell detects an external stimulus it releases the introns that correspond to the chemicals detected.  All of these introns become available to be spliced into RNAs simultaneously thereby allowing for these introns to be spliced together to form memory RNAs.  Introns that are not available at that time do not get spliced into these RNAs.  An alternate theory is that the introns are, rather, bound together end to end.  This provides a ready chemical explanation for general and specific memory (explained later) by the cell controlling the length of such chains of introns, with small chains forming to produce general memory and long chains for specific memory.  However, the neural version of this theory appears to fit the evidence better, and further, the chain theory requires the existence of an additional molecule for binding and releasing introns.  Now, if these RNAs are available for splicing all the time, then the information spliced into them would soon be spliced out, with the experiences of the moment being spliced into their place.  In order for memories to last, RNAs must be blocked from the actions of splicers shortly after the memories are stored on them.  In DNA the action of molecules on the DNA strand is blocked by its mirror strand that is usually bound to the chemically active sights on that DNA.  This binding of two mirror DNA strands together (the double in double helix) ensures that normally, there is no part of the DNA that is exposed that reacts strongly to other molecules.  In this way, the body can regulate the DNA’s production of RNA by controlling when the strands part, and also, by making the DNA chemically non-reactive, chemical reactions that might damage the genetic material are minimized, increasing the longevity of an individual’s genetic structure.  By manufacturing a mirror RNA, similar to the way DNA reproduces itself, an RNA can gain the same benefits, protecting itself from splicers and increasing its longevity.  Besides recording and storing a memory you must also be able to retrieve it.  You need to experience a few cue stimuli and have these stimuli cause you to recollect all the other stimuli that occurred along side those stimuli at a past time.  Moreover, it’s desirable that the more stimuli that are available, the more likely the event will be remembered.  When the cell separates the RNAs from their mirror RNAs in order for the intron splicers to gain access to them, introns are quickly released from all the memory RNAs.  This leads to a relatively equal number of every intron that cell produces, which is useless for remembering a specific memory.  The release of these memory RNAs, however, does makes it easy for the cell to produce a new memory at that time.  The key to recollection of memories is in the mirror RNAs.  When the mirror RNAs are released they will proceed to produce mirrors of themselves, thereby producing new memory RNAs.  However, if a few introns are in abundance in the cell as a result of the actions of sensory proteins, these introns can be fitted into the memory RNAs being generated from the mirror RNAs, and thereby, increase the rate of production of those specific RNAs.  Once the memory RNA is produced, its introns are spliced out, and as a result, the concentration of the introns that coincide with those specific memories, increases.  The more introns in a memory RNA that coincide with the introns that are being released by the sensory proteins, the faster production of these RNAs will be from their mirror RNAs.  As a result, the memories that are closest to what is currently being experience by the cell will be recollected the strongest.

            Within a single celled organism this type of memory is of limited use since it only acts to give the cell the ability to react to anything that might indicate a predator or prey.  Effectively, the cell has a nose and memory but no intelligence, just evolved reactions with which to use them.  However, within a multi-cellular organism this nose can be used to detect the operation of other cells.  Since most chemical reactions are reversible, these sensory proteins can also produce or release the same chemicals they detect.  In this way, a memory cell can detect and remember the behaviour of the entire body, and then, at a future time, output these memories to the body causing it to repeat its past reaction.  Within complex multi-cellular organisms the memory cells are specialized to receive input from a limited, although large, number of cells, each giving off one or very few chemicals that the memory cell can detect.  In this way, individual cells within the body can be specialized to detect specific stimuli.  Once this stimulus is detected by one of these specialized sensory cells it sends a signal that releases one specific chemical to the memory cells, resulting in the activation of that chemical’s one intron.  The result is that the memory of this cell is converted from its original function of remembering the chemicals in its environment to remembering the outputs of sensory cells.  This takes memory out of the chemical world and into the macroscopic world of large multi-cellular organisms i.e. us.  Now, the distances between the sensory cells and the memory cells would make the transmission of chemical signals unacceptably slow.  In order to deal with this problem neural pathways are used, with axions being sent from cells that read the signals of the sensory cells to the memory cells.  These sensory neurons give off the particular chemical signature of their corresponding sensory cells when they activate, and thereby, tell the memory cells exactly which sensory cell initiated the signal.  Since axions typically operate in only one direction the memory cells shouldn’t be able to return a memory directly.  If a memory cell was to use an axion to send its signal, it would only be able to send its response to one of the neurons that it receives its information from.  This is the case since the introns necessary to release the proper chemicals cannot travel through the axion at any significant speed, so the axion cannot be connected to all the sensory neurons, it has to be set up to release only one chemical.  This could still work if the memory RNAs are able to transfer between memory cells (this ability is vital for recognition functions of the brain) so that a number of cells all contain the same memories.  In this way, each memory cell could send a piece of the memory, so that together, the whole memory gets sent.  Alternatively, a memory cell could be surrounded by a large number of neurons equivalent to the sensory neurons, each with a return connection to its respective sensory neuron.  Because of their close proximity to the memory cells, the distance could be traveled by the introns in a short enough time.  Once one of these neurons was activated, it would rapidly send its signal through its axion to its corresponding sensory neuron.  However, the rule of axion directionality isn’t absolute; the first set of sensory neurons in vertebrates send axions that branch with one end going to the sensory cells and the other to the second set of sensory neurons.  So, the signal is sent backwards from the sensory cell, then switches to forwards at the branch to reach its destination.  Although, in this case, the signal still always goes in one direction, this shows that axions can send signals both ways.

            Although, in complex organisms, introns are used extensively to store stimuli from the sensory cells, they’re still essential for the control of gene expression.  That memory and gene expression both act through the same system is the basis of psychosomatics.  An example of psychosomatics is of an individual who lives on a mountain for a substantial period of time.  Spending this time in an oxygen deprived environment would lead to their body adapting by increasing lung and cardiovascular capacity.  The increased activity of genes involved in this adaptation produces increased levels of the introns connected with those genes, while the stimuli of the mountainous environment produces the introns connected with those stimuli.  The result is that the individual’s memories of their stay on the mountain also contain memories of the way their body adapted to that environment.  After many years living at sea level, their body would loose its adaptation, but if they spent time remembering that mountainous environment, as would typically happen if they spent considerable time planning a return trip, then these memories, acting over a sufficient amount of time, would result in re-adaptation.  Effectively, they would remember the genes necessary to be adapted to that environment and hence would output the proteins for greater lung and cardiovascular capacity.  As well as this adaptation, psychosomatics also explains the placebo effect.  If you can convince an individual that a medicine will make them healthy then they will think and act like a healthy person, and hence output the proteins they normally output when healthy.  This may make them feel good for awhile, but it’ll reduce their adaptation to their real situation, the situation of ill health, and thereby potentially give their disease the upper hand.  Among the gene expressions that psychosomatics can modify are the genes involved in antibody production.  In homeopathy a significant dosage of a chemical is introduced to the body, a chemical the body attempts to disable by outputting antibodies.  The memory of the adaptation to this chemical is connected to the memory of taking it.  At a future time, when the individual has a particular illness that those antibodies could deal with, they can take a placebo of the chemical and, believing they actually took the chemical, their body would output those antibodies.  Since there would be no chemical in the body to use up the antibodies, they’d act exclusively to fight the illness.  Homeopathy fails to work for doctors since their patients rarely knows what they’re being given and usually pays little attention to the medicines they receive.  Without this knowledge or attention, the memories necessary for homeopathy to work are absent.  The individual who practices homeopathy on themselves forms the necessary memories; however, it’s the misconception that lower doses are in fact higher doses, a basic belief of homeopathic practitioners, that allows the placebo to work.  This necessary belief in a falsehood, however, acts to destroy the credibility of such people.  It’s possible to get around these problems.  The basis of homeopathy is the connection of a stimulus with an antibody reaction.  A substantial stimulus, such as a unique design or smell, would be much more interesting and memorable than a homeopathic substance’s name, and as such, would be effective for use on the average patient.  Moreover, a name produces little stimulus and therefore has to compete with the amount of stimulus produced by the knowledge that the placebo is not the actual chemical.  A strong and interesting stimulus presented with or instead of a placebo could override the small stimulus created by the awareness that the chemical is not present, and thereby remove the need for deception.  A significant problem with psychosomatics is that the body specializes only a few tissues within the brain to memory.  Consequentially, most of the body’s cells, including the antibody cells, are separated from the direct sensory stimulus provided by the neural pathways, making it difficult for them to attach external stimuli to their adaptations.  However, chemical signals from the sensory cells could potentially provide some basic experience of the outside world.

            Besides the stimulatory system, the system of neurons between the sensory and memory cells, there are three other basic types of neural systems involved in the proper function of memory cells.  The first is the excitatory system.  In order for memories to last, the memory RNAs must remain bound to their mirror RNAs; and yet, to remember a memory, the memory RNAs must be separate from their mirrors.  Therefore, it’s necessary for there to be a system by which memory RNAs are normally bound to their mirror RNAs, but that under certain circumstances the RNAs are separated to allow access to the cells memories.  Now, these memory RNAs don’t just control memories, they also hold the introns that regulate the expression of the cells genes, and further, many messenger RNAs may also be bound to mirror RNAs, consequentially being rendered inactive.  As a result, the same conditions that release memories also release the RNAs that control the activity of the cell, so, when the cell isn’t remembering anything, it’s also metabolically relatively inactive, producing vary little protein, whereas when it’s ready to remember, it‘s quite active.  This state of metabolic activity, which we generally call excitement, is important for dealing with important situation where greater activity can allow the cell to avoid danger or take advantage of an opportunity; but these are the same situations in which memory is most valuable, both to take advantage of past experiences and in order to make memories of the event for future use.  When there’s relatively little going on, either beneficial or detrimental, the cell’s best strategy is to remain as dormant as possible to preserve its resources and to put its memories into their most stable state, which is when the memory RNAs are bound to their mirrors and hence inaccessible.  In macroscopic creatures, this stimulus, like that for memories, must be transmitted through neural pathways from sensory cells to the memory cells.  I generally call these two paths the stimulatory and excitatory pathways.  The simplest of the excitatory senses is pain.  When pain is experience, this sensation activates an excitatory pathway which acts to excite some of the memory cells.  Once the cells are excited, the memory RNAs become separated from their mirrors and, as a result, begin to degenerate.  It is this degeneration, the destruction of the memory cells’ memories, that causes the displeasure of pain.  However, a given pain only activates a few memory cells and a large number of memory cells aren’t connected to the pain neural pathways, so pain cannot normally damage the memories that make a person’s personality.  What makes pain distinct is that it activates without regard for any other stimulus the individual is experiencing, which is also why it’s the simplest of the excitatory pathways, it’s not connected to anything else.  The other excitatory pathways are either activated by the stimulatory pathways, causing the memory cells to activate when there’s something to be remembered, or they activate stimulatory pathways, allowing the memory cells to use the excitatory stimulus to make memories.  The result is that when the memory cells are excited, causing their memories to degenerate, the cells are producing more memories to replace the old ones.  If the net amount of memory is increasing, then the sensation will usually be that of pleasure, whereas if the net memory is decreasing, the experience is typically displeasant.  The sensation of pleasure and displeasure are the result of the phenomena of consciousness (this phenomena is well out of the scope of these documents) and there’s some complexity to the circumstances under which it expresses these sensations.  Since pain is experienced separate from stimulus (that which forms memories) the excitement of pain is usually not accompanied by the creation of memories, so most peoples’ experience of pain is displeasant.  This, combined with the fact that many pains are to severe to be countered by any amount of stimulus and that many forms of injury prevent the experience of stimulus without greatly increasing the pain, results in people generally equating pain with displeasure.  However, like the other forms of excitement, pain can be pleasant if it’s accompanied by sufficient stimulus.

            Although degeneration of memory RNAs is greatest when cells are in an excited state, some degree of desatement (degeneration) occurs at all times.  The rate of desatement of particular stimuli is chosen by evolution in-order to deal with the purpose of those stimuli.  Sight desates very, very slowly since it’s used for long term memory, sound, intermediately to create a moderate need for communication but to allow for reasonably long memory, touch desates rapidly to demand periodic attention to the body while taste and erogenous touch desate even quicker so as to maintain a strong need for food and sex.  Evolution also uses the nature of the excitement inducing the desatement to control behaviour.  For example, when hunger is experienced it excites taste-based memories causing them to desate.  This desatement creates a need to experience taste and hence satisfy the hunger. 

            The second system is the generalization system, which controls the degree of generality/specificity of memories.  Control of generality and specificity is important in that, if all your memories were specific, although you could remember specific events in your life, you wouldn’t be able to generalize the meaning of those events.  For instance, you could remember every chair you ever saw but you couldn’t use the word chair to describe one you’ve never seen before because you’d lack a general understanding of what a chair was.  Likewise, if your memories were all general you wouldn’t be able to remember anything specific about your life.  What distinguishes generality from specificity is the amount of memory components used to trigger a memory.  If the brain sends a detailed image, composed of numerous memory components to the memory cells, there will probably be only one memory that coincides with that image.  So, the strongest memory being output by the memory cells will be that specific image.  If only a general image, composed of few memory components, was sent to the memory cells, there’d be many memories that coincide with that image, all of which would be outputted simultaneously.  The result of many memories, all being sent together, is that the components of these memories that are the same will accumulate to make those component’s signals strong, while those that are different between the many memories would produce weak signals.  The strong components are then the generalized memory, consisting of those elements of memories that always coincide with that particular input.  For instance, the input ‘chair’ would output many different colors and materials, but it would always output an object whose proper function is to support a sitting individual.  Now, throughout the nervous system are numerous inhibitory neurons.  When an individual experiences a moderate level of stimulation, there is little problem with the nervous system handling this, but when the stimulus increases, neurons may be forced to fire excessively.  Excessive activation of neurons drains them of energy and other resources and will eventually kill them.  To prevent this, the inhibitory cells detect the activity of the neurons around them and, if they receive excessive stimulation from any of these, activate and thereby inhibit them.  A similar process can be used to produce generality/specificity.  An inhibitory neuron can be connected to a number of the sensory neurons that connect directly to the memory cells.  As more of these sensory neurons are activated, the inhibitory neuron becomes increasingly excited, sending a larger inhibitory signal to all the neurons it’s connected to, thereby reducing, but not necessarily stopping, their activity.  In this way, only a limited number of these sensory neurons can be activated, with those that have the weakest signals being edited out.  In order to control the level of generality, these generalization cells only need some type of control over their general level of activity.  For instance, a chemical released by the brain could act to excite the generalization cells and thereby cause them to increase the number of sensory neurons that they inhibit, thereby increasing the generalization of all memories.  An absence of this chemical would cause memories to be specific.  Likewise, variation in the generalization cells throughout the brain could allow some areas to deal with general thought while other areas would deal with specific memories.  The action of generalization cells of editing out the numerous random, weak signals that are output by general memories also serves to ensure that only the strong, meaningful signals remain.

            The third system, the recognition system, is more difficult to understand than the previous ones.  Recognition, as used here, is the ability of the brain to distinguish two stimuli as being of the same type despite they’re activating vary different neurons or the same neurons in vary different patterns.  The simplest examples of this are displacement, rotation, and size of an image, in which the image or the components of that image appear, at two different times, at very different locations on an individual’s eye.  If these two experiences of the image overlap then some of the visual receptors and their corresponding neurons will be used to recognize part of the image, and then, later, to recognize a different part of that image.  It is therefore impossible for the brain to use a simple one intron per one receptor system to recognize images since it would only take for the image to land one or more receptors out on the retina from a past experience, to activate a completely different set of introns.  It’s only in the case of chemical memories, such as smell and taste, that this simple system works sufficiently.  The solution to complex recognition can be understood if you accept that memories can be exchanged between memory cells.  This process is simple in the case of intron memory since the memories are stored in the cytoplasm of the cells, so, all the memory cells have to do is form vacuoles, which will contain some of their cytoplasm, and absorb the vacuoles of the other cells.  The ability to exchange memories is important because it allows these memories to be handled by memory cells that have vary different neural connections with the sensory cells, and, as a consequence, encode and interpret the memories differently.  For the most part, in complex organisms, sensory cells do not activate a specific intron in the memory cells; smell and taste are the most significant and distinct exceptions to this.  Rather, the introns are activated by the neurons that are directly connected to the memory cells, so that a specific neuron will activate the same intron in any and all memory cells it’s connected to.  The neurons that connect to these intron specific neurons, the simplest of which transmit signals from the sensory cells, have no such order to them, they can connect to any of these neurons, and, as a result, end up activating any intron.  Now, in the example of an image that is seen twice, the first image will activate a set of neurons that activate a specific set of introns in a memory cell, thereby forming a memory of the image.  This memory is then, over a short period of time, transferred to the other memory cells, after which this image is seen a second time, but displaced a small distance to the side on the retina.  The image then activates a different set of neurons, neurons that activate a different set of introns and which also send their axions to a different memory cell, a cell set up to recognize an image with that particular displacement.  This memory cell achieves this recognition by taking the memory RNA it received from the original memory cell, but the neurons that feed it its input are such that they activate the same introns but receive their input from receptors that are displaced from those that fed the original memory cell.  In this way, the second cell recognizes the displaced image as the same as the original.  Since a given memory cell coincides with a particular change in the location or appearance of an image, the precise cell(s) that are activated can tell the brain precisely what change from the original or normally experienced image, occurred.  Now, there are many ways in which the intron specific neurons could connect to the memory cells, but only a few of these connections would correspond to a change in an image.  So, in order for this recognition system to work, there must be a system by which the connections that allow the brain to recognize things are the ones that are generated.  What is distinct about connections that produce recognition from those that are random is that they produce and receive greater activity.  A memory cell with good connections, connections that allow it to recognize images that it’s receiving memories about from other memory cells, will recognize things more often, and hence, will output a larger amount of stimulus through its reciprocal connections to the neurons that feed it.  Moreover, if a connection is good then the results of a memory will make sense and will thereby generate further activity in the brain.  The more a neural connection is used the stronger it gets, so, since a good connection promotes greater activity through itself, directly or indirectly, it becomes stronger, whereas random connections weaken and eventually disconnect.  All the brain has to do is make occasional, random connections between the intron specific neurons and the memory cells so that there are neural connections in the first place to reinforce or brake.

            This is a simplification of recognition for the purpose of explaining the basic concept.  When an individual observes an object, every memory cell that receives input from the activated sensory cells is activated.  This produces huge numbers of different memory RNAs which all express the same memory.  However, for pretty much any given memory cell, all of these memories simply represent different ways of seeing the image.  Later, when the image is seen again, large numbers of memory cells will be activated, but the majority of these will find a memory RNA that coincides with this different view of the same object.  The result is that all of these many memory cells will be putting out the same response to that image, for instance its name or significance.  Besides displacement, rotation and size there are a number of other important adjustments to a stimulus.  One is a particular type of warping of an image.  If you take a picture and hold it perpendicular to your vision you see the image in its ideal form.  However, if you were to rotate it, everything in the image would scrunch up, looking thinner than it actually is, and yet you have no trouble recognizing the contents of the image.  This ability is used all the time to recognize anything that has rotated.  All the brain has to do to handle this case is to have a number of memory cells develop neural connections that coincide with such a warping of an image.  Other visual adjustments to a stimulus are variation in color and shade.  These can be handled by either creating memory cells with neural connections that coincide with various different colors and shades or by creating memory cells without any color or shade connections.  In this second case, the cells recognize the image without reference to its color or shade, they simply don’t see these characteristics, however, such cells wouldn’t give the individual the ability to tell if and by what degree the image has changed in these qualities.  Likely, both techniques are used in the brain.   Sound is identified in a similar fashion to vision.  The ear sends signals of a sound in the form of numerous individual frequencies, a given neuron only transmitting a single frequency.  This is a much more useful way of dealing with sound than the way it’s dealt with by modern circuitry, but a microphone of this type would be much harder to create.  Once the sound reaches the memory cells, it’s treated like a visual image, only, instead of being two dimensional it’s one dimensional, a line going from the smallest frequencies to the largest ones.  The memory cells can recognize if this sonic image is displaced, i.e. whether a higher or lower frequency voice is saying the same thing.  Likewise, changes in the intensity of the sound and any important warps in the sonic image are easily dealt with.  Beyond this, the memory cells receive input from the touch and proprioceptive sensors of the body, from the balancing receptors of the inner ear and from various parts of the brain.  If there are any meaningful patterns in these inputs, the memory cells will find them as well.

Spinal Cord and Reticular Formation

            The common perception of muscular motion is that of an electric motor.  As current’s applied, the muscle moves continuously towards a particular angle.  When the muscle reaches the desired position, the current is turned off.  An alternate view is of a solenoid with a piston.  When current is applied the piston moves rapidly from one precise position to a second.  The muscles are set up like bundles of many small solenoids, each one of which can move a muscle only a minute distance, but when working together, can produce a significant contraction.  Moreover, numerous nerve fibres feed a single muscle and the more fibres that feed a muscle the finer that muscle’s control.  This suggests an on/off behaviour is used to control a muscle.  If the intensity of the nerve was being used to position the muscle then few nerves would be necessary; the body could send a few nerves down the nerve tracts and then magnify the impulse using a ganglion at or near the muscle.  Also, more nerves shouldn’t increase the precision of the muscle since they would only increase the number of routs for the signal to take.

By activating a precise number of nerve fibres, the individual can make a muscle contract to a precise position.  In this way, when a person wants to take on a specific posture, all they have to do in remember the associated nerve fibres and then allow their body to act on that memory.  Their body will react as a whole without the need for any further adjustments.  When a person wants to turn a doorknob, the associated memory is of the nerves necessary to put their hand in contact with the knob.  When their hand contacts the knob the sensation activates a second associated memory of the nerves that produce a grasping hand.  The sensation of grasping, contact with a doorknob and a desire to open the door then induces a recollection of the nerves that produce the posture of a turned hand, so their hand moves to that posture.  Martial artists sometimes talk of imagining your fist as being beyond or through the target; this is because it’s the ultimate position of the arm, not the process of getting the arm to that position, which makes a punch.         

This view of the nervous control of the muscles is not sufficient to explain all movement.  By a purely postural view of movement, if you place your arm at your side and then raise your hand at the elbow your arm should move fastest at the bottom and top positions and slowest when it’s at a right angle to your body when it’s experiencing the greatest gravitational effect.  You can make your arm behave this way by relaxing it, but normally it moves evenly across the arc of motion without any difficulty.  This behaviour is produced by the stretch reflex arc.  As force acts on the muscle, the neuromuscular spindles send excitatory impulses to the alpha motor neurons in the spinal cord.  These impulses don’t increase the number of alpha neurons that are active but instead increase the strength of their signal to the muscles.  By sending a more intense signal to the same muscle cells their contraction is intensified, increasing their resistance to an external force, but the degree of contraction of the muscle and hence the position of the limb are unchanged.  The primary use of this reflex is for balance.  As the body shifts from equilibrium, a force is produce on the opposing muscles; the spindles detect this force that’s moving the muscle from the chosen posture and react by increasing the force of these muscles.  Further, as force is relieved from other muscles, they reduce the force they exert.  Consequentially, the forces in the muscles that would promote regaining balance are increased and the forces pushing the individual’s body off balance are reduced.

            The intensity of the stretch reflex is controlled by gamma motor neurons which transmit to the neuromuscular spindles.  By increasing the gamma motor signal, an internal force is applied to the spindles causing them to act as though there’s an additional, non-directional, external force.  The spindles react by sending a signal of the combined internal and external forces to the alpha neurons.  In this way, the muscles tense up to resist an imaginary, non-directional force, but still react to the real force and thereby maintain a uniform motion.  Relaxation of the gamma motor neurons is likely the primary means of relaxing the muscles to produce the rag doll effect of reduced resistance to gravity.  Precise control of the gamma reflex is used to produce a number of muscular skills.  The distinction between many martial arts is a matter of which gamma reflex skills they’ve developed or emphasize.

            The gamma motor neurons are also used to manipulate the more complex gearing reflex.  This reflex involves a signal from the neuromuscular spindles traveling through the cerebellum to the cortex and back to the muscles through the alpha motor neurons.  By making the spindles act as though they’re under a greater load, this reflex responds by gearing down the muscles motion.  I explain the precise operation of this reflex when explaining the cerebellum.

            Another important reflex is the flexor reflex.  This reflex is used primarily as a component of the instinctual learning and sympathetic expression mechanisms of the nervous system, but it’s also used directly as a stop reflex.  If an individual moves their hand towards an object, it moves freely until contact; at this point the muscles of their arm lose strength in the direction of movement, reducing the pressure of impact.  The flexor reflex operates by touch receptors activating de-excitatory neurons in the spinal cord.  These de-excitatory neurons then reduce the intensity of the alpha neuron’s signal to their muscles.  In this way, the muscles in the direction of movement lose power, but still try to go to their commanded posture.  Immediately after this, pressure on the neuromuscular spindles activates the gearing reflex, which changes the cortical output to the alpha neurons to that of a posture that just touches the object.  Since a given posture is specific to a single position of an object being touched, this cortical output is also used by the brain to identify the object’s location. 

By controlling the level of excitement of the de-excitatory neurons in the spinal cord, an individual can regulate the response of their flexor reflex, even turning it off.  The stretch reflex, on the other hand, has no such intermediate neurons.  The stretch reflex is active so long as the alpha neurons are active, and can only be modified by manipulation of the neuromuscular spindles’ output.  In addition to deactivating the flexor reflex, an individual can force a limb through an object by either beating the reflex, (moving their limb too fast for the reflex to activate in time to soften the impact) by putting so much momentum into the limb that turning off the muscles won’t significantly reduce the impact or by using an impact point that lacks this reflex (the back of the hand is set up to soften a blow from an arm that’s moving to the side, not forward, as in a punch). 

There is also the common jerk response created by the flexor reflex.  When an individual is excited (such as when concerned or worried about an expected experience) the gamma motor neurons to the spindles are activated to increase the tension of the muscles.  Upon contact the flexor reflex de-excites the alpha neurons to the muscles that flex the limb toward the contact’s direction.  This de-excitation relaxes one set of muscles but leaves the opposed set excited, thereby causing the limb to jump back.  This response is deactivated by either relaxing the muscles (inhibiting activation of the gamma neurons) or by deactivating the de-excitatory neurons of the flexor reflex in the spinal column.

The instinctual learning and sympathetic expression aspects of the flexor reflex are caused by the body becoming excited in particular ways, to particular stimuli, and then having this excitement deactivated by physical sensations.  A simple example is in the opening and closing of the hand to touch and grasp an object.  When an individual desires to touch an object, i.e. feeling it, the nerves that transfer the sensation from the receptors to the upper brain excite to make them sensitive to this sensation.  When these nerves are excited, the nerves to the muscles of the back of the hand (in the case of an expected sensation on the front of the hand) are excited.  This causes the hand to favour an open position.  On contact, the flexor reflex deactivates this muscular excitement and thereby causes the hand to close on the object.  An infant doesn’t know the precise signals to send to their limbs in order to open and close their hand, and doesn’t understand that an open hand can fit around an object and a closed hand can grip this object.  This reflex allows them to successfully perform the grasping action without understanding it, and thereby learn from the experience.  Since the infant doesn’t have a successful and consistent signal to send to their muscles, this reflex dominates their behaviour; once the muscle positions are understood, this reflex only effects the strength of the action, not the action itself.  In adulthood, the behaviour of opening the hand when expecting a touch on the front of the hand remains since the reflex makes moving in this manner easier.  When we see someone open their hand and we have reason to believe that the individual expects to be touched on, or to touch with, their palm, we recognize that the individual’s palm is excited.  This recognition expresses itself as a sympathetic response; the same areas of our brains that are involved in excitement of our palms are used to understand the same experiences in others.  Consequentially, when we recognize this excitement in another, it induces the same excitement in us, although to a lesser degree.

There also appears to be an active reflex similar to the receptive one I just described.  In this case, if the individual desires to hold something (this is an action, not a perception), instead of the opposed muscles being excited the muscles in the direction of the object of the desire are excited.  In this way, when the infant wants to touch an object, their fingers spread out, and then, when they want to grasp the object, contact with the object relaxes the spreading muscles and the desire to grasp excites the grasping muscles, giving them the strength to hold the object.   This reflex is more apparent in the case of the back and legs.  When a person wants to look at something they typically stand or sit up straight.  A person who is disinterested or relaxed will slouch; they have to be excited by that which they’re looking at for these reflexes to be active.  On the other hand, if the individual is working on something, they typically sit and lean over the thing they’re working on.  So, when a person is experiencing something, they maintain straight legs and back, but when they’re active, they pull their legs in and slouch over that which they’re focused on.  A walk is basically a mixture of these two reflexes.  As the person walks they are attempting to make something in the distance closer so that they can better experience it.  This desire to experience the far away object causes one leg to straighten backwards, thereby pushing the person towards the object.  The connection between the eyes and the legs can be seen in the common behaviour of standing on ones toes in order to try to see farther or better.  The desire to carry out the action of walking causes the other leg to be bent and pulled forward towards the object, similar to a reaching reflex of the arm.  Since the bottom of the foot is part of the back of the leg, when the foot lands, the front muscles that bend and pull the leg forward are deactivated by the flexor reflex.  The leg tries to straighten and push back until the foot leaves the ground and the front muscles can excite again.  Since this reflex is excitatory and is therefore not involved in precise positioning of the legs, it is only involved in learning to walk and in maintaining the strength of the legs during the act of walking.  Once walking is learned the positioning of the legs is dealt with by the cortex.

I’ve used the concepts of excitement and stimulus in discussing the operation of the muscles.  Excitement of a muscle involved control over the intensity of the signal going to the muscle, where as the stimulus was the precise number of neurons, and thereby the number of muscle cells, that were active in order to produce a precise flexion of the muscle.  This is a fundamental concept in understanding the nervous system.

The receptive component of the spinal cord and peripheral nervous system is likewise split into these two parts, the excitatory and the stimulatory receptor systems.  Neither system is completely excitatory or stimulatory in nature.  Both systems send stimulatory information to the thalamus, the excitatory system sending the sensations of pain, light touch, heat and cold while the stimulatory system sends a variety of touch sensations, most of these going to the ventral posterior nucleus (VP) with some of the excitatory systems stimulatory fibres going to the posterior thalamic group.  The VP thalamic nucleus takes these stimulatory inputs and projects an image of the sensations onto the cerebral cortex.  The excitatory system’s projections through the posterior group, although stimulatory in nature, function to modify the purpose and operation of parts of the cortex.  This is what distinguishes the excitatory and stimulatory systems. The primary purpose of the stimulatory system is to produce an image of the world, while the primary purpose of the excitatory system is to modify the operation of the nervous system, with the biggest exception to this rule being the addition of excitatory stimulus to the stimulatory system’s fibres to the VP nucleus.

Now, the primary expression of the excitatory systems manipulation of the nervous system is not through its action through the posterior thalamic group, but rather through the reticulus (central group of reticular nuclei).  The reticulus is the primary excitatory organ; it receives stimulus primarily from the excitatory system and excitatory fibres from the premotor cortex, particularly, but not exclusively, for the cortical excitation of sensory pathways and motor reflexes.  All this information is moderately generalized so that a localized excitatory input can effect a substantial enough area of the body; it’d be of no value for a pinprick to excite only one motor neuron since this wouldn’t be enough to promote any response.  The information is then sent out from the reticulus to the spinal cord and brain-stem to excite the sensory, motor and reflex areas, and to the intralaminar thalamic nuclei, which distributes fibres to much of the cerebrum, similar to the posterior thalamic group, and thereby allowing the cortex to respond to the level and nature of the individual’s excitement.  In addition to this, the reticulus activates excitatory fibres to memory cell organs through the intralaminar nuclei and through the locus coeruleus, and thereby generates the experience, although not necessarily the rational awareness, of pain, and controls the degree of formation and recollection of many types of memories.  Further, the locus coeruleus, and thereby the reticulus, has strong control over the level of activity of much of the higher brain and the autonomic systems.

Besides the behaviour of the excitatory system’s sending stimulatory fibres to the cortex through the thalamus, there are a number of other exceptions to the general division of the sensory systems into excitatory and stimulatory.  The flexor reflex involves the excitatory system acting in a stimulatory fashion by stimulating de-excitatory neurons to deactivate the motor neurons.  Now, the proprioceptive system is distinct from the standard stimulatory system since it sends most of its fibres through a separate pathway through the cerebellum before they reach the thalamus to finally create an image of the body’s position on the cerebrum.  Although the proprioceptive system follows a separate path, it still acts predominantly in a stimulatory fashion.  The exceptions to this are the branches of the proprioceptive fibres that act to excite the primary motor neurons within the stretch reflex, and also branches ending in the spinal cord to activate the excitatory system in a way that’s identical to the standard excitatory receptors.  These branches to the excitatory system allow it to handle proprioceptive sensations as well as the basics, pain, light touch, heat and cold, so that stretching and muscular stress also induce direct excitement.  The final significant exception to the excitatory, stimulatory division is the lower raphe (raphe nuclei of the medulla).

The operation of the lower raphe can be shown through a simple experiment.  Take your arm and brush a fingertip across it as lightly as possible, this works best if the arm has been uncovered for a while; the sensation should be sharp.  Take your other hand and rub your arm thoroughly, and then brush your fingertip across it again.  This sensation will be dull.  The lower raphe operates by being activated by both the excitatory and stimulatory systems, and then acting by sending out inhibitory signals to the cerebellum, autonomic system and sensory and motor areas of the spinal cord and brain-stem.  The inhibition of the cerebellum and motor areas acts to reduce reflexive motions, which is important when the raphe induces sleep and relaxation.  Likewise, inhibition of the autonomic system promotes sleep and relaxation.  The inhibition of the sensory areas, which are part of the excitatory system, but not the stimulatory system, acts to reduce the excitatory stimulus through the excitatory system.  The loss of this stimulus acts to directly reduce stimulus to the cerebrum through the inactivity of the stimulatory components of the excitatory system, but also reduces the activity of the reticulus, and thereby reduces the activity of the upper brain and memory cell organs, reducing their ability to experience stimulus.  Consequentially, when you rub the skin, the activity through the sensory pathways acts to activate the raphe, which then acts to inhibit the experience of excitatory stimulus and thereby reduce, directly and indirectly, your experience of stimulus.  Since the lower raphe is activated by the stimulatory system, but doesn’t deactivate this system, rather deactivating the parts of the brain this system attempts to stimulate, the raphe remains active despite the lose of sensitivity.  The primary purpose of this system is to allow people to not focus on things that they’re continually touching.  When you sit, the sensation of sitting acts to de-excite the parts of your body that feel that sensation, so that shortly after sitting you can focus on whatever you’re doing.  For land creatures, which are always in contact with something, i.e. the ground, this operation of the raphe is vital to maintaining focus on things of importance.

Two common uses of this property of the nervous system are scratching and the wearing of clothing.  When the individual becomes focused on an irritating sensation, i.e. an itch, the act of scratching induces a great deal of stimulus, which then acts to de-excite the skin at that location, thereby ending the itch.  Clothing acts to stimulate large areas of an individual’s skin so that it de-excites.  This de-excitation makes it difficult for the skin to become excited, preventing the individual from becoming sensually or sexually excited, either spontaneously or as a result of others looking at their body, and thereby prevents embarrassment and discomfort.  From this, it would seem that cloths would make people asexual, being insensitive to sensual/sexual matters, but the lack of attention to attaining stimulus allows the individual to desate their body, thereby increasing their needs.

            Besides the excitatory/stimulatory division, the excitatory system can be further divided into positive and negative excitatories.  Positive excitatories are tracts that act to excite the sensory tracks that carry the stimulus to the memory cell organs.  Because tracks of these sorts only increase the amount of stimulus that reaches memory cells, increased positive excitement acts to increase the level of pleasure.  However, without the ability to increase the sensitivity of the memory cells themselves, positive excitatories cannot produce intense pleasure, they only act to produce a generally good mood.  Negative excitatories are excitatory tracks that act to excite the memory cells directly, but don’t activate the sensory pathways.  Pain is a strong negative excitatory in that it excites, and hence causes degeneration of, memory cells without increasing the stimulus the cells receive.  Negative excitatories commonly produce displeasure, however, if they are balance with positive excitatories so that the level of excitement of the memory cells is proportional to the amount of stimulus being experienced, then these negative excitatories allow for ecstasy.  Consequentially, positive excitatories produce mild, good emotions while negative excitatories produce great emotional highs and lows.  Like the distinction between the excitatory and stimulatory systems, there are few excitatory fibres that fall exclusively under positive or negative; never the less, this distinction is psychologically useful.

Oculomotor System

            The muscles of the eye are like other muscles in that they take on a precise position dependent on the nervous signal sent to them.  However, they don’t need neuromuscular spindles or other muscular systems to determine position and stress.  Since the eyes experience no external forces on them, there are no unpredictable stresses and those that do exist are small, and further, the position of the eye is that which the brain gives it since the eye travels exceedingly fast from one position to another.

            In order to position the eye on an object of interest you need to know how far the object is from the position the eye is currently in, i.e. the number of degrees right, left, up or down, and you need the eye’s current position, i.e. number of degrees from looking straight ahead.  The brain sees the eye’s current position as the muscle position signal the motor cortex is sending to the eyes.  The object of interest’s position is seen as the location on the person’s visual cortex that they’re focused on.  The image the person sees is mapped out on this cortex and if something appears on this cortex that is exciting (bright, strongly coloured, contrasted, or is associatively exciting, i.e. desirable, fearful, ect.) then that excitement makes that something the individual’s focus.  The memory cells observe the motor neurons that are active and the part of the visual cortex that is excited, and from past experience remember the motor neurons that were active after an eye movement and the new position of the excitatory stimulus after such a movement.  When the individual desires to put the focus at the centre of their visual cortex for better viewing, this desire appears in the cortex as an excitement at the centre of the visual cortex.  The memory cells read the current position of the eyes in the motor cortex and the current focus, in the visual cortex, plus the desired focus, and from past experience remembers, and then, consequentially, activates the correct motor neurons necessary to centre the eyes on that focus.  Because this method relies on RNA memories it is slow and unreliable, but it does allow for successful positioning of the eyes until the cortical reflexes are developed, which is important the learning of these reflexes.

            The cortical reflexes involve a different type of memory cell, one that learns by trial and error.  As the individual becomes accustomed to focusing their eyes on objects, the cortical fibres produce a large number of connections between locations of potential stimulus on the visual cortex and potential, resultant muscular positions of the eyes in the motor cortex.  Every muscle position that ever produced centring of an interesting image in the cortex has cortical connections to that imaging part of the cortex, so when an image is seen in the future this image activates many different muscle positions at the same time.  For instance, an individual may have had two instances in which an interesting image appeared 20° left of centre in their cortex.  One instance involved their eyes being straight ahead so successful centring of the image on the cortex involved the eyes moving to 20° left.  Another instance involved their eyes being 20° to the right, so successful centring involved looking straight ahead.  In the future, when an image appears at 20° to the left on their cortex, fibres in their cortex will activate both a 20° left and a straight ahead eye position.  Because these reflexes involve large cortical fibres, with no unreliable, slow chemical memories, they can respond exceedingly rapidly, but they send to much information.  This is where the second variety of memory cells comes into play.  The way in which these memory cells work is that they take in the situation and indicators of success or failure, in the form of pain and stimulation, and output an inhibitory signal.  If the cells receive a great deal of stimulus around the time they put out their response, they strengthen that output, but if little stimulus is experienced, or a need for stimulus is created by pain, then they weaken.  In this way, they learn the precise cortical motor fibres to shut down in order to produce a desirable, and avoid an undesirable, situation.  So, well before a stimulus (image) attracts your attention, the stimulus of the position of your eye is read by these trial and error cells which respond by deactivating every cortical pathway between the visual cortex and the motor cortex that would not lead to a correct positioning of the eyes.  When a stimulus catches your eye, the part of the visual cortex this image appears in activates its cortical fibres to the motor cortex, but only the fibres that would produce the right positioning of the eyes are unblocked, so the eyes move to that position.  Because the memory cells are used in preparation for a reflex, not the reflex itself, they don’t decrease the reflexes speed.

            A second form of eye motion is tracking, where the eye smoothly follows the object of interest.  There are two forms of tracking.  One is where you move your head and your eyes remain fixed on a stationary object.  In the other, the head is stationary and the eyes move with a moving object.

            The first type of tracking involves the semi-circular canals.  When the head is rotated, the receptors in the canals put out a signal that increases in intensity (increased number of receptors being activated, less sensitive ones activate with fastest movements) with increased rate of rotation of the head.  This information is sent to the motor nuclei of the eye where it excites the neurons that position the eyes.  In this way, if the head is turned gently, the eyes try to reposition themselves as the object moves from the centre of their vision, but since the excitatory stimulus they receive from the canals is small, they reposition themselves with little force and hence little speed, but the object is only moving across their vision slowly.  If they move their head fast then the excitatory stimulus the muscles receive is large and the muscles reposition the eyes fast, which allows the eyes to keep up with the fast moving image.

            For excitement of the muscles in the case of the stretch reflex calibration of the intensity of the reflex could be attained through the gamma loop.  If the brain needed a stronger reaction, it could increase activity to the gamma fibres feeding the neuro-muscular spindles.  In the case of the eye muscles calibration of the intensity of motion is vary important, without it the eyes would lag behind or move faster than the object they’re tracking.  However, I’m not aware of any direct connections between the cortex and this reflex pathway.  There is every reason to believe that the cortex acquires information from the semi-circular canals (through the cerebellum) and this does allow for one type of calibration.  Among the stimuli the memory cells can take in when determining the muscular positions of the eyes to produce is the degree of excitement of the canal receptors.  If the eyes must be moved faster, the eyes can be displaced a shorter distance thereby increasing the force of their motion.  If the eyes are moving to fast, the displacement can be lengthened.  These changes in displacement won’t cause the eyes to miss their target since, for moving an image, it’s the rate of motion, not the position the eyes are going to that effects whether they maintain themselves on their focus.  Only when the image stops does the position the eyes are going to matter.  Another possibility is that the cortex receives information from the canals and, instead of directly affecting the intensity of the excitatory pathways between the canals and the oculomotor nuclei, the cortex instead, just adds on to this excitatory stimulus, sending excitatory as well as stimulatory fibres to the oculomotor nuclei.

            Most objects in the world don’t move or move vary little, so most of the images that move across our vision are the result of our own movements.  So, the first type of tracking is the most important and the evolutionary development of the assistance of the semi-circular canals in understandable.  For the second type of tracking another technique for following an image must be available since the canals provide no information about the movements of other objects.

            In order to track an object purely by sight it is necessary for the brain to somehow measure the rate of travel across the eye (degrees per second) and then turn this information into a muscular excitement so that the eyes muscles can move at the correct rate.  However, the memory cells do not possess any sense of time.  Everything that occurs while the memory RNAs are forming is all clumped together with no reference to what came first or second.  In order to detect the order of events memory cells use a sequence of inputs and outputs.  The person sees a stimulus which causes them to remember something, but that memory acts as a stimulus causing them to remember something further.  This sequence can be long and complex and is the fundamental basis of reasoning.  This type of thought has no direct connection to time and so, can’t be used to measure the rate of anything that occurs exceedingly rapidly.  Depending on the number of steps and the time between individual memory RNAs activating, which may vary significantly, an act of reasoning will take a particular period of time to complete.  This period of time is relatively long and unreliable and, as such, can only be used to estimate macroscopic periods of time.  Memory cells can detect the time of a particular memory by using an external stimulus, such as a clock, and adding the observed time to the other stimuli in the memory, but this requires a particular stimulus that is unique to each moment of time and no such stimulus exists in the body.  Further, this would require complex (from a memory cells point of view) calculations in order to work out the rate of something’s movement from these memories.  The one way a memory cell could figure out the rate of travel of something is by noting some change in the appearance of that thing as a result of its movement.  A memory cell must be active for a period of time, long enough to form complex memories but short enough to get on to the next observation or reaction.  As a result, when an object is traveling across a stationary eye, the memory cells will absorb the image along its course of travel.  Consequentially, the image will appear elongated, smudged, but also transparent since the memory cells will see the object when it’s over a location and when it’s not at the same time.  The degree of elongation, smudge and transparency will be unique to a given rate of travel across the eyes (degrees per second) for a given length of time that the memory cells are active.  If the memory cells are active longer, these qualities will be greater since they’ll absorb the image for a greater period of time, and visa versa.  So, so long as this period is set, or the memory cells can detect the period of time they’re active, which would likely be related to the level of excitement of the cells, something that is easy enough for them to deal with, then they can determine the rate of movement of an image.

            When the eyes are moving with an object, the object doesn’t appear to be moving across the eye.  At this time, the memory cells will detect the level of excitement being sent to the eye muscles and will thereby know the rate of motion of the object and, as well, the correct excitement to send to the eye muscles (the same amount that was sensed).

            The second form of tracking seems as though it might interfere with the semi-circular canal type, and further that this first type might be unnecessary in the face of the second type.  The stimulus of the inner ear and that of seeing a moving object are from distinctly different sources and, as such, don’t add together.  If both sources are telling the eyes to move at the same rate, then the eyes will follow the orders of both sources and move at that rate, not twice that rate.  However, this only relates to semi-circular canal signals that got to the cortex, not the ones that excite the oculomotor nuclei directly.  As the head is rotated, the excitement of the eye muscles produced by the canals reduces the amount of excitement that needs to be produced by the memory cells observing the moving object.  However, these cells can detect the signal from the canals (through the cerebellum) and, as a result, can respond by putting out less excitatory signal.

            The reasons the canal type of tracking exist are firstly, that in the early evolution of the brain learning to track by sight took too long and was too complex for short lived, simple creatures.  Secondly, most objects were stationary, so developing substantial brainpower for something infrequently used may have been a waste.  Thirdly, it may simply be much faster than the second type of tracking and hence too valuable to get rid of.  Fourthly, it adds to the stimulus of the other type of tracking to make tracking more reliable under the circumstances it’s most frequently used.  And fifthly, for learning.  It would be difficult for a child to learn image recognition if every time they moved, images streaked across their vision.  Canal based tracking allows the child to track most objects immediately, thereby allowing them to learn how they look.  Once the child knows how objects should appear, then they can see how those objects change when they move and from this can develop a sight based tracking.

            The final type of oculomotor functions are focusing and binocular vision.  Each eye has eight muscles, six motor muscles around the eye, one muscle surrounding the lens which allows change in its shape and one iris muscle to moderate the amount of light entering the eye.  Besides moderating light intensity the iris can increase the sharpness of an image by contracting.  This can help overcome imperfection in the lens of the eye.  There is little evidence that the iris is intentionally used in this fashion, although sight on a bright day is clearer than on a dark day.  Of the six motor muscles, two deal with horizontal motion (left and right); the other four are more complicated.  If you turn your right eye all the way to the right for instance, two of these muscles would move the eye up and down, the other two would turn it clockwise and counter-clockwise.  Turning this same eye to the left, the second pair would move the eye up and down while the first pair would move it clockwise and counter-clockwise.  When the eyes are centred, a combination of two of the four muscles working together can produce up, down, clockwise and counter-clockwise movements.  To produce these movements the eyes have to remember different muscle positions for every left to right position of the eyes.

            The eyes readily rotate to maintain the same position with respect to gravity; if you rotate (tilt) your head one way, your eyes rotate the other.  In this way, when we see an object we see it in relation to the direction of gravity.  Although our brains can identify an object that is rotated as the same object, this doesn’t necessarily give us the ability to distinguish what angle an object is in.  To distinguish the angle of rotation we need some reference point for the object to be tilted from.  In the case of a person, we normally see people in the upright position, so, if an individual is leaning, the memory cells will recognize them as a person, but they will draw on memories of an upright person to do so which allows the memory cells to tell us how far from the norm the person is angled.  If the eyes didn’t keep a constant angle (tilt) with respect to gravity then the images of people (or other objects) would be seen in many different angles and so our ability to tell people’s angle with respect to gravity would become vary inaccurate.

            In the movement of the eyes, we always move our eyes together up and down but we are able to move them in opposed, sideways directions for binocular vision.  The muscles that move both eyes up when the eyes are facing to one side are controlled by the same hemisphere of the brain, while the muscles that move both eyes down are controlled by the opposite hemisphere.  Since the eyes are moved together up and down, always focusing on the same things, the brain equates a movement of one eye as the same as a movement of the other.  In this way, when the memory cells set the position of one eye, the other takes on the equivalent position automatically, thereby making independent movement generally impossible.  However, since the opposing muscles (down muscles for up muscles) are controlled by the opposite hemisphere, they do not necessarily take on a particular position with respect to each other.  The separation of the hemispheres prevents equating a contraction of an upward muscle with the relaxation of a downward muscle.  This is distinctly different from other muscles of the body where a muscle on one side of the body moves independently of muscles of the other side, while the opposed muscles (muscles where one must expand in-order for the other to contract) on one side of the body are controlled by one hemisphere, so that consequentially, the brain equates the contraction of one muscle with the relaxation of the other.  Because of the way the eyes are set up, it’s possible to command the eyes to go both up and down, rotate clockwise and counter-clockwise, by giving different commands with each hemisphere.  This allows opposed muscles to be contracted or relaxed simultaneously, which acts to distort the eyeball and change its focus. 

The lateral eye muscles are controlled through two different neural pathways; for a given eye, one pathway controls both of these muscles from one hemisphere while the other pathway controls each from opposite hemispheres.  In this way, the brain can use these muscles both to distort the eyeb