IN THIS ISSUE of the Archives, the article by Duman and colleagues1 helps clarify the next layer of understanding of the neurobiology of depression and, ultimately, brings to light more powerful and selective treatment interventions. As in the catecholamine and indoleamine hypotheses of the 1960s, Duman et al appropriately rely heavily on a pharmacological bridge to better understand potential alterations in depression based on the effects of antidepressant medications. In addition, microstructural alterations in the brains of patients with depression have begun to be reported, with initial reports of increased expression of corticotropin-releasing hormone in the brains of suicide victims who had depression; increased size of the pituitary and adrenal glands; and a variety of findings concerning receptor, peptide, and structural alterations in the hippocampus, including preliminary findings of decreased hippocampal size as a function of duration of prior depressions.2 It is against this background that tracing the effects
Post RM. Molecular Biology of Behavior: Targets for Therapeutics. Arch Gen Psychiatry. 1997;54(7):607–608. doi:10.1001/archpsyc.1997.01830190025003
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