This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Manji, H. K. Articles by Potter, W. Z. Search for Related Content PubMed Articles by Manji, H. K. Articles by Potter, W. Z. Social Bookmarking                   What's this?

ECT treatment does not enhance neuroendocrine responses to serotonergic challenge

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

John K. Hsiao

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

Emile D. Risby

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

Ossama T. Osman

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

Matthew V. Rudorfer

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

William Z. Potter

Section on Clinical Pharmacology, Clinical Neuroscience Branch, National Institute of Mental Health, Bethesda, MD 20892, USA

We prospectively investigated the effects of a course of electroconvulsive therapy (ECT) on neuroendocrine responses to serotonergic challenge in five depressed patients. Low dose intravenous chlorimipramine (CMI) challenge produced a modest release of prolactin and significant increases in plasma adrenocorticotrophic hormone (ACTH) and cortisol. Interestingly, ECT did not alter the neuroendocrine responses to serotonergic challenge despite clinical response in four of the five patients. If anything, the modest prolactin (PRL) response to CMI, rather than being enhanced, appeared to be abolished following ECT. Using confidence intervals, we estimate that there is less than a 5% probability of a 78% increase in prolactin response to CMI after ECT. To detect this, a sample size of greater than 35 would be needed. These findings suggest that neither ECT nor the clinical response in severely depressed patients is likely to produce consistent changes in neuroendocrine response to the acute serotonergic effects of CMI infusion. The lack of effect of ECT on prolactin response to serotonergic challenge might be explained by simultaneous enhancement of both serotonergic and dopaminergic neurotransmission.

Key Words: electroconvulsive therapy • serotonin • depression • chlorimipramine

Journal of Psychopharmacology, Vol. 6, No. 4, 501-508 (1992)
DOI: 10.1177/026988119200600405


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?