In my post, "The Genius Gene," I referenced the limbs, or processes, of neurons, which are known as axons and dendrites. What I did not mention, is that both axons and dendrites branch off into smaller processes of themselves, and axons specifically terminate in what are known as terminal buttons. These buttons then form what are called synapses with one of the dendrites, cell body (or "soma"), or even an axon of another neuron (how synapses are created will be discussed in a later post). A synapse formed by a terminal button and a dendrite is axodendritic, one formed by a button and a soma is axosomatic, and one formed by a button and an axon is axoaxonic (Use the below visual as a reference). Chemicals known as neurotransmitters are released by terminal buttons when the rest of the neuron is stimulated by a communication from a sensory input or another neuron, and are the neurons' primary method of information transmission. Released neurotransmitters will briefly float through the space between the button, and the surface it has formed a connection with, known as the synaptic cleft, and consequently affect the dendrite, soma, or axon of whatever neuron with which the synapse had been formed. The newly affected neuron will then either propagate or inhibit the transmission which caused the original release of chemicals into the synaptic cleft, and this depends on the type of the neurotransmitter. This will continue, from neuron to neuron, until the transmission is inhibited, or completes the communication of the information being transmitted.
Three synaptic connections: leftmost is axodendritic, center is axosomatic, rightmost is axoaxonic |
In my post entitled "Subjective Perception," I had discussed what I stipulate to be the nature of consciousness, a phenomenon which I had referred to as multiphasic cognitive relay. Essentially this term entails the requirement for a sensory system to be processing information that corresponds to information currently being processed by other sensory systems in order for the individual to become aware of the information. In the previous paragraph, I had said that before a behaviour becomes habitual, it is still planned and initiated consciously. The frontal lobe, responsible for the planning of behaviours (among other things), communicates with the other three lobes of the cerebrum: the temporal, parietal, and occipital lobes. These lobes are responsible for processing their corresponding sensory information, possibly storing that information as memory, and then associating previously stored sensory information with either that which is currently being perceived, other memories, or plans the frontal lobe might be formulating. I will refer to this process of association as cognitive association, and the frontal lobe employs thus each time it attempts to create a plan. In the case of a behaviour which is not habitual, I stipulate the individual is conscious of cognitive association relative to the given situation because the brain is using multiple different cognitive faculties in order to process the sensory inputs of the situation. Furthermore, I convict that the individual is not conscious of the initiation of habitual behaviour because of the pathological development that caused the efferent and afferent neurons that communicated information on same or similar previous occasions where perception and response, on the part of the given individual, was consistent, to display neuroplasticity and alter their synaptic connections in order to "predict" similar transmissions of information. Therefore, only one sensory input would be necessary in order to at least begin the efferent transmission of information to the brain, where the same cognitive association would occur, and the same afferent motor neurons would be triggered, thus resulting in a habitual behaviour. This would also account for conscious interruption of a habit, that if another sensory system receives an input from the situation whilst the first sensory input is being processed or the motor neurons are carrying out the consequent behaviour, the individual will become aware of the process.
Neuroplasticity entails the alteration of synaptic connections on the parts of involved neurons. However, what had the original state of the synaptic connections been, before any processes displaying neuroplasticity had occurred? In my previously referenced post, "The Genius Gene," the brain of the child learning basic addition creates what I referred to as intellectual precedents that correlate to the basic postulates that are needed to prove the legitimacy of addition. And just as the infant needs to begin experience what is known as stereoscopic vision (vision with both eyes) early in their life, I hypothesise that it is at this point in the child's life, it also experiences the emotional reactions to different situations of those around him, for example his parents, and his brain then creates intellectual precedents which correspond to those emotional reactions, and uses them as a basis for how the child himself will feel in relation to different situations. After that initial intellectual precedent, neuroplasticity can occur repeatedly and alter the way in which the individual will feel about the same or similar situations, or situations which remind him of the ones in which he witnessed his parents respond emotionally, as an infant.
As in my previous posts, I will reference both the plausibility as well as hypothetical nature of my stipulations. What is interesting to note, however, is that my idea as to how emotions originate within individuals correlates to what I have recently discovered to be the most generally accepted theory of emotion within the scientific community: the James-Lange Theory. I will actually go more into detail concerning the actual nature of emotions, or irrational thought processes, in later posts, as well as all else I made clear I would discuss further. I also suggest you read my previous posts if you have not already, because I use each one as a reference point in this post, and I will continue to do so in future entries.
References
Carlson, Neil R. Physiology of Behavior. Boston: Allyn and Bacon, 2011. Print.
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