Serotonin

Although less studied, in conditioned fear experiments animals demonstrated an increase in serotonin (5-HT) turnover in different brain areas, with preferential release in mPFC. Serotonin antagonists produce behavioral deficits resembling those seen following inescapable shock. Chronic stress increases cortical 5-HT2 receptor binding and reduces hippocampal 5-HT1A receptor binding. Drugs that enhance serotonin neurotransmission are effective in reversing this behavioral "learned helplessness." Injection of serotonin into the frontal cortex after stress exposure reverses behavioral deficits.

The effect of stress in activating serotonin turnover may stimulate a system that has both anxiogenic and anxiolytic pathways within the forebrain. A primary distinction in the qualitative effects of serotonin may be between the dorsal and median raphe nuclei, the two midbrain nuclei that produce most of the forebrain serotonin. The serotonergic innervation of the amygdala and the hippocampus by the dorsal raphe are believed to mediate anxiogenic effects via 5-HT2 receptors. In contrast, the median raphe innervation of hippocampal 5-HT1A receptors has been hypothesized to facilitate the disconnection of previously learned associations with aversive events or to suppress formation of new associations, thus providing resilience to aversive events.

Conquering Fear In The 21th Century

Conquering Fear In The 21th Century

The Ultimate Guide To Overcoming Fear And Getting Breakthroughs. Fear is without doubt among the strongest and most influential emotional responses we have, and it may act as both a protective and destructive force depending upon the situation.

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