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Amygdala

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Amygdala


In: Causes

The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Sensory information enters the amgydala through the nuclei of the basolateral complex (consisting of lateral, basal, and accessory basal nuclei). The basolateral complex processes sensory related fear memories, and communicate their threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices.

Another important area is the adjacent central nucleus of the amygdala, which controls species-specific fear responses, via connections to the brainstem, hypothalamus, and cerebellum areas. In those with general anxiety disorder, these connections functionally seem to be less distinct, with greater gray matter in the central nucleus. Another difference is that the amygdala areas have decreased connectivity with the insula and cingulate areas that control general stimulus salience, while having greater connectivity with the parietal cortex and prefrontal cortex circuits that underlie executive functions.

The latter suggests a compensation strategy for dysfunctional amygdala processing of anxiety. Researchers have noted "Amygdalofrontoparietal coupling in generalized anxiety disorder patients may .. reflect the habitual engagement of a cognitive control system to regulate excessive anxiety." This is consistent with cognitive theories that suggest the use in this disorder of attempts to reduce the involvement of emotions with compensatory cognitive strategies.

Clinical and animal studies suggest a correlation between anxiety disorders and difficulty in maintaining balance. A possible mechanism is malfunction in the parabrachial nucleus, a brain structure that, among other functions, coordinates signals from the amygdala with input concerning balance.

Anxiety processing in the basolateral amygdala has been implicated with dendritic arborization of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborization. By overexpressing SK2 in the basolateral amygdala, anxiety in experimental animals can be reduced together with general levels of stress-induced corticosterone secretion.