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Mental disorders
Depression and Manic Depression
Alzheimer’s-type Dementia

The irrational fear that characterizes phobias may have been conditioned in the individuals concerned without their having any conscious memories associated with it. One explanation offered for this phenomenon is that the circuits of the amygdala mature before the circuits in the hippocampus that are responsible for conscious memory. An implicit emotional memory could thus become established without any explicit memory's being associated with it.

The circuits of the amygdala receive information about the functional status of the body's various internal organs. The amygdala may then relate the pieces of information about the various organs to one another by amplifying the effects of the sympathetic nervous system through its efferent pathways. A person might perceive this activation of his sympathetic nervous system consciously and then have an explicit memory that these physical symptoms represent the onset of a panic attack. Knowing that a panic attack was coming would make this person even more anxious, thus setting the vicious cycle of the panic attack in motion.


Though the amygdala appears to play a central role in all anxiety disorders, some studies seem to indicate that conditioned fears and generalized anxiety disorder involve different circuits in the amygdaloid nuclei.

In the case of conditioned fears, the circuits involved appear to be located in the lateral nucleus and the central nucleus of the amygdala. Consequently, these neural pathways are believed to play an important role in those anxiety disorders, such as phobias, that involve specific stimuli.

In contrast, non-specific anxiogenic signals appear to be handled by a neighbouring region, the bed nucleus of the stria terminalis. Thus this nucleus would be associated with anxiety disorders of more diffuse origin, such as generalized anxiety disorder or panic disorders (see sidebar).

If these observations are confirmed, they could open up interesting possibilities for new treatments, because if there are any biochemical differences between these two nuclei (for instance, in their receptors or neurotransmitters), researchers might be able to design anxiolytic medications that were more specific to and effective for each of them.

The specific pathways emerging from the amygdala, as well as those entering it, have already been targeted by psychoactive medications such as the benzodiazepines (Valium, etc). These substances reduce the symptoms of many anxiety disorders by potentiating the natural inhibiting effect of certain neurons (GABAergic neurons, for example). The potentiated effect of these neurons raises the threshold for triggering anxiety, so that stimuli that would normally be anxiogenic will no longer produce the negative emotional responses usually associated with them.

It is thought that anxiolytic medications may also reduce anxiety by acting on the hippocampus, where they would suppress the emergence of anxiety-producing explicit memories.


Obsessive-compulsive disorder seems to be associated with a defect in a neural circuit that runs from the frontal lobe to the central grey nuclei, then on to the thalamus, and finally back to the frontal lobe. This defect might be attributable to genetic factors, or possibly to immunological ones, since obsessive-compulsive disorder sometimes appears after a streptococcal infection.

Link : Quelles sont les origines des Toc ? Link : OCD and Streptococcal Infections Linked
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