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Psychological Physiology in Social Anxiety Disorder and Shyness

Ruy Miranda
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To understand the probable neurophysiological action mechanism of medication and psychotherapy in Shyness and social phobias, it is necessary to understand the neurons' language. We will review now how the impulses go from one nervous system cell, a neuron, to another.

The neurons are large cells with many projections (dendrites) from the cellular body. These projections extend from a few microns to sometimes as much as a meter.

Any function, such as thinking, moving, sleeping, looking, or feeling, involves the integration of an unknown number of neurons in specific brain areas, as well as the nervous structures of the organisms outside the brain. The neurons interconnect in complex chains. The message travels through each neuron as electric impulses. All indications point to the fact that the impulses are transmitted in the same way in all the neurons, that is, as electric signals.


March of Impulses


The electric signals are ions (atoms or group of atoms that received or lost electrons) with positive and negative charges formed along the neuron as a result of chemical and physico-chemical reactions. These reactions terminate in some place of the neuron membrane. Some particularities:

* A few ions stay in the interior of the neuron; others stay outside.
* These ions move from the interior of the neuron to the outside and from the outside to the interior of the neuron through pores in the membrane.
* The ions with positive charge are potassium, sodium and calcium ions. The largest are potassium ions.
* Chemical and physico-chemical reactions cause electric currents in the neuron.
* These reactions end at some point of the neuron.

How is information passed on in the form of electric signals to the next neuron?

The passage is through substances called neurotransmitters.

What a neurotransmitter is – A neurotransmitter is a substance that transmits a signal in the nervous system, including the brain, from one neuron to another or others. It is necessary because the electric current does not cross the small space that exists between two connected neurons. That substance is stored in the neuron that produced it in a region called pre-synapse. It passes the electric impulse from one neuron to the another in a region called synapse.

Synapse – It is made up of structures of two connected neurons. Each neuron has many structures for connections at different points of the projections from the cell body (dendrites), as well as at the end of a long projection (called axon).

Let us imagine a segment of such an electric current. A neuron, which we will call neuron A, is situated in any position in a neuron chain. Neuron A binds itself to neuron B, which binds itself to neuron C and so on successively. To put this into a scheme:

Neuron A – Synapse – Neuron B – Synapse – Neuron C – etc.

 

In order for the electric impulse from neuron A to go to neuron B, the intermediation of a substance in the synapse is necessary because the reactions terminate at some point of the membrane. That substance is a neurotransmitter. The same thing occurs in the passage of the impulse from neuron B to neuron C and so on. To put this into a scheme:

Neuron A – Neurotransmitter – Neuron B – Neurotransmitter – Neuron C – etc.

 

Thus, the neurons are messengers of positive and negative electric signals (the signals of the ions). Neuron A— just as B and C and all the others in a sequence—neither thinks nor makes decisions. It is as "dumb" as the computer you are using, i. e., it only transmits positive and negative electric signals. Let us put it into a scheme:

Electric impulse in the neuron A – Neurotransmitter in the synapse – Electric impulse in the neuron B – Neurotransmitter in the synapse – Electric impulse in the neuron C – etc.

 

Particularities in the passage of the impulse from one neuron to another – The neuron membrane, as well as that of any other cell, is made up of substances (molecules) organized so as to leave spaces (pores) through which substances needed for cell survival and the exercise of special functions come in and go out SELECTIVELY. These molecules are different from those that originate the ions and respective electrical charges in the neurons. On the other hand, the pores are different in the vicinity of the synapses. These are the reasons why the electric impulses terminate in some place of the membrane, near the synapse.

The impulse in neuron A that reaches the synapse regions discharges or activates the neurotransmitter, which, in turn, binds to certain structures (called receptors) of neuron B's membrane. This connection triggers the reactions in neuron B. So, we say that the neurotransmitter bears a chemical signal.

Neuron B receives the chemical signal and starts the chemical reactions that generate ions with positive and negative charges. These reactions go in the direction of the synapse with neuron C. And the process repeats itself.

You can see the alternation of electric impulses and chemical signals. Let us put it in a scheme:

Electric impulse in the neuron A – Chemical signal (neurotransmitter) in the synapse – Electric impulse in the neuron B – Chemical signal (neurotransmitter) in the synapse – Electric impulse in the neuron C – etc.


Neurotransmitter Production


Neuron A produces a neurotransmitter in a region close to the synapse with neuron B and discharges it in the synapse. Neuron A, which passes the stimulus on to neuron B, is known as the proximal neuron, while neuron B is called distal.

Neuron B produces a neurotransmitter in a region close to the synapse with neuron C and discharge it in the synapse. Thus, neuron B is proximal as regards neuron C and neuron C is distal vis à vis neuron B. Neuron C will be distal as regards neuron D and so forth and so on. Thus, all the neurons produce neurotransmitters. Besides passing a chemical signal, all of them receive a chemical signal.

The structure of the distal neuron in the synapse where the chemical signal comes in is called receptor.

Neurotransmitter regulation – There is a regulation of the amount of neurotransmitter in the synaptic space. It seems to be made in the proximal neuron. In addition to producing the neurotransmitter in a region close to the synapse, the proximal neuron injects more neurotransmitters into the space or removes eventual excesses and stores them. That regulation by the proximal neuron would involve:

– production of the neurotransmitter;
– storage of the neurotransmitter close to the synapse;
– discharge of the neurotransmitter in the synaptic space;
– re-uptake of the neurotransmitter and re-storage.

In certain cases the neurotransmitter is de-activated (changes its chemical structure) just after it passes the stimulus to the distal neuron. When the proximal neuron comes in contact with the following stimulus, the neurotransmitter is re-activated.


Locations Liable to Have Flaws


One can deduct where problems may occur:


*disorder in the production of neurotransmitter in the proximal neuron;
*the proximal neuron does not inject enough amounts of neurotransmitter in the space, in spite of having them stored in its interior;
*the proximal neuron injects an excessive or insufficient amount of neurotransmitter into the space;
*the proximal neuron does not adequately activate the neurotransmitter;
*the proximal neuron does not adequately remove the neurotransmitter from the space;
*the synaptic space ends up with too much or too little neurotransmitter;
*the distal neuron displays chemical or physical-chemical alteration in the structure situated in the membrane in the synapse region, called receptor;
*alteration in the receptor "distorts" the electric signal when it arrives as a chemical signal, through the neurotransmitter, to the distal neuron.

It is impossible, with current instruments, to know which defect occurs in any person. You can see the long list of possible defects; and there are more which are not included here. However, whatever it may be, the exactness of the signal transmitted by the neurotransmitter becomes compromised. It is possible that the evolution of nanotechnology will provide some information in the near future.

Neurons A, B, C, D, and all the others have a greater number of synapses. Indeed, one single neuron can have thousands. Example: 6,000 synapses. You can imagine the extremely complex network of 100 billion computing units (neurons) inter-connected by thousands of synapses.

If one or more of these defects occur in a set of neurons exercising the same function, the messages will be distorted. Examples: A defect in the set of neurons involved with humor may lower humor (depression) or raise it (elation, mania); another set involved with the state of alertness may lower it (inattention) or raise it (excessive attention, apprehension, anxiety and possibly Shyness and phobias).

It is expected that medications correct those defects in Shyness and social anxieties. However, as we don't know where the defect is, the action of one medication can be good for a given person and ineffective for another.

Neurotransmitters, Plasticity of the System, Psychotherapy

Neurotransmitters and Psychotherapy – To indicate psychotherapy for problems which may result from chemical reactions may seem paradoxical. Yet, psychological problems do affect neurotransmitters outside of the brain—and probably in it too. Example: The expectation preceding a school exam can alter the activity of the neurotransmitter that regulates the bladder's sphincter so that the student urinates several times . Likewise, perceiving a strange person as threatening and judging yourself unable to confront him (one of the so-called psychological problems) could affect the activity of neurotransmitters in some specific region. Changes in these two beliefs ("the strange is threatening" and "I am unable to confront him") could lead to some changes in the activities of the neurotransmitters or in the related structures. Psychotherapy can promote changes like that.

Plasticity of the System and Psychotherapy – On the other hand, the extensive neural network has a property called plasticity. At the core, plasticity is a constant change in the ways of the ion currents. In the day-to-day activities, the synapses that inter-connect the imagined neurons A,B,C and D in our example are not fixed. On the contrary, they change constantly. Such change is necessary to maintain the dynamic equilibrium (homeostasis) proper to any living system. It is believed that the re-direction of the electric currents underlies what we call learning and memory, and that learning stimulates the formation of new ways for the flows. And all psychotherapies are, at the core, a learning process that must stimulate such new ways.

It may be now understandable why many professionals think that it is better to combine psychotherapy and medication in Social Phobia/Anxiety and in severe Shyness.


Electric Flow and Genes


There is evidence that some psychological problems have a genetic basis. Some cases of Shyness and Social Anxiety are among them. The possible explanation for this fact can be in specific genes, called "pacemaker current," concerned with the encoding of ion channels (pores in the membrane). Mutations in these ion channel genes might contribute to some disorders, caused by a lower plasticity of the system. For these cases, if the evidence comes to be confirmed, we depend on the discovery of new families of medication.

In another article, we will see how this information can help to understand how the antidepressants act.


May, 2004.


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This web site, the Social Anxiety Disorder and Shyness Directory and these articles contained on this web site are not solicitations, are not medical advice and are not intended as medical advice. This web site, the Social Anxiety Disorder and Shyness Directory and these articles are intended to provide only general, non-specific medical information and are not intended to cover all the issues related to the topics discussed. This web site, the Social Anxiety Disorder and Shyness Directory and these articles do not create any physician-client relationship between Ruy Miranda and you, and they do not replace the eventual relationship between you and your physician, psychologist, or other healthcare professional. This article’s author recommends no particular medication and does not represent the interests of any person, company or pharmaceutical laboratory.


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You may want to read other articles on Social Anxiety Disorder / Social Phobia and Shyness:

Basic Articles:

Self-Concept/Self- Actualization – Shyness Nucleus

Self-concept, Body Image, Self-depreciation and Shyness

Shyness and Social Anxiety Disorder: Neurophysiological Approach

Shyness Articles:

What Is Shyness? Fear, Anxiety, Anguish?

Questions and Answers on Shyness

Humiliation Stories, School Spankings: Examples of Shyness Causes

Social Anxiety Disorder Articles:

Social Anxiety Disorder: What It Is, The Anxiety Attack Symptoms

Social Anxiety Attacks: Incidence, Onset, History, Evolution

Social Phobia / Anxiety Disorder: Treatment

Social Phobia / Anxiety Disorder: Differential Diagnosis

Avoidant Personality Disorder

Medications in Social Phobia: Side Effects - Part 1

Antidepressants Tricyclics: Side Effects - Part 2

Metabolic Pathways Individual Differences and Medications Side Effects - Part 3

Genetic Changes: Medications Side Effects - Part 4

First Line Antidepressants - Side Effects - Part 5

Social Anxiety and Shyness Articles:

Panic Disorder, Shyness, Social Phobia - Differences

Why Self-Help in Shyness and Social Anxiety Disorder / Social Phobia Doesn’t Help You

Shyness and Social Anxiety Disorder:Medication Action

Facial Blushing, Redness of the Face, Ears and Neck

Psychoses, Shyness and Social Phobia


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