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State and trait abnormalities in serotonin function in major depression

University Department of Psychiatry, Warneford Hospital, Oxford, UK

Correspondence: Professor P.J. Cowen, University Department of Psychiatry, Warneford Hospital, Oxford OX37JX, UK

Declaration of interest None. Funding from the Medical Research Council.

Background Neuroendocrine studies of brain serotonin (5-HT) function in depression generally show evidence of impaired 5-HT function but it is disputed whether or not this impairment resolves with clinical recovery.

Aims To use the endocrine response to the selective 5-HT reuptake inhibitor, citalopram, to study brain 5-HT function in acute and recovered depressed subjects relative to healthy controls.

Method We used a double-blind, placebo-controlled design to measure the prolactin and cortisol responses to citalopram (10 mg intravenously) in patients with major depression, in unmedicated subjects recovered from depression and in healthy controls.

Results The prolactin responses to citalopram were blunted similarly in both acutely depressed and recovered subjects. The cortisol responses were blunted in the acutely depressed patients but not in the recovered subjects.

Conclusions Our data support the proposal that some aspects of impaired 5-HT neurotransmission may be trait markers of vulnerability to depression. The recovery of the cortisol response to citalopram may indicate resolution of hypothalamic—pituitary—adrenal axis dysfunction.

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