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...

Full description

Saved in:
Bibliographic Details
Published in:Journal of psychopharmacology (Oxford) 2007-11, Vol.21 (8), p.885-887
Main Authors: Hesketh, S.A., Leggett, J.D., Jessop Henry, D.S.
Format: Article
Language:English
Subjects:
Adrenal gland diseases
Adrenal glands
Adrenal Glands - drug effects
Adrenocorticotropic hormone
Animals
Antidepressants
Biological and medical sciences
Citalopram
Citalopram - pharmacology
Corticosterone
Corticosterone - blood
Cosyntropin - pharmacology
Drug therapy
Exposure
Hypotheses
Male
Medical sciences
Neuropharmacology
Pharmacology. Drug treatments
Physiological aspects
Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer
Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)
Psychology. Psychoanalysis. Psychiatry
Psychopharmacology
Rats
Rats, Sprague-Dawley
Rodents
Serotonin Uptake Inhibitors - pharmacology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0269-8811
1461-7285
DOI:10.1177/0269881107078310