Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1-24) in rats.
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.
Hesketh
S A
SA
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, UK.
Leggett
J D
JD
Jessop
D S
DS
D000311:Adrenal Glands / Q000187:drug effects*; D000818:Animals; D015283:Citalopram / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood; D003366:Cosyntropin / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology*
D015283:Citalopram; D003345:Corticosterone; D003366:Cosyntropin; D017367:Selective Serotonin Reuptake Inhibitors