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. Author manuscript; available in PMC: 2010 May 1.

Published in final edited form as: Prog Neurobiol. 2009 Feb 7;88(1):17–31. doi: 10.1016/j.pneurobio.2009.01.009

AD are hypothesised to increase serotonergic signaling at the postsynaptic 5-HT_1A receptor either by desensitizing the somatodendritic 5-HT_1A receptor in the raphe, or by facilitating the activation of G proteins by the postsynaptic 5-HT_1A receptor. Normalized signaling at the postsynaptic 5-HT_1A receptor reduces cortisol and CRH release, restores endocrine function, and improves mood.

AD are hypothesised to increase serotonergic signaling at the postsynaptic 5-HT_1A receptor either by desensitizing the somatodendritic 5-HT_1A receptor in the raphe, or by facilitating the activation of G proteins by the postsynaptic 5-HT_1A receptor. Normalized signaling at the postsynaptic 5-HT_1A receptor reduces cortisol and CRH release, restores endocrine function, and improves mood.