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Journal of Psychopharmacology
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0269881107078310v1
21/8/885    most recent
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Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats

S.A. Hesketh

Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, UK

J.D. Leggett

Department of Anatomy, University of Bristol, Bristol, UK

D.S. Jessop Henry

Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, UK, david.jessop{at}bristol.ac.uk

We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained due to increased adrenal sensitivity to lower ACTH levels. To test this hypothesis, we intravenously injected ACTH (1—24) to rats (dose 3 ng/rat) exposed to citalopram through minipump infusion for 14 days and to control rats (no citalopram). ACTH significantly increased plasma corticosterone levels in both control and citalopram treated rats over a period of 120 min. There was no significant difference in plasma corticosterone between citalopram treated rats and control rats at any time point. Therefore we conclude that, under these experimental conditions, citalopram does not appear to sensitize the rodent adrenal gland to ACTH, and that other mechanisms may be responsible for the ACTH/corticosterone disconnection.

Key Words: SSRI • citalopram • ACTH • corticosterone • rat

This version was published on November 1, 2007

Journal of Psychopharmacology, Vol. 21, No. 8, 885-887 (2007)
DOI: 10.1177/0269881107078310
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