Strain-dependent neurochemical and neuroendocrine effects of desipramine, but not fluoxetine or imipramine, in Spontaneously Hypertensive and Wistar–Kyoto rats

Strain-dependent neurochemical and neuroendocrine effects of desipramine, but not fluoxetine or... Spontaneously Hypertensive rats (SHRs) and Wistar–Kyoto (WKY) rats differ in their emotional responses to stress and antidepressant administration. We have analysed different neurochemical and psychoneuroendocrine responses to repeated pretreatments with fluoxetine, imipramine or desipramine (10 mg/kg p.o. daily for 4 weeks) in SHRs and WKY rats exposed to a daily 2-h restraint episode for the last 5 days of antidepressant administration. Following a 24-h wash-out period, WKY rats displayed higher plasma antidepressant and antidepressant metabolite levels than SHRs. Fluoxetine pretreatment decreased ( 3 H)citalopram binding at midbrain serotonin (5-HT) transporters, whereas tricyclic and/or fluoxetine decreased ( 3 H)ketanserin binding at cortical 5-HT 2A receptors, ( 3 H)CGP-12177 binding at cortical ß -adrenoceptors, and ( 3 H)nisoxetine binding at midbrain noradrenaline (NA) transporters in both strains. None of the antidepressants affected ( 3 H)8-hydroxy-2-(di- N -propylamino)tetralin binding at hippocampal 5-HT 1A receptors. In WKY rats, repeated restraint triggered a desipramine-sensitive 140% increase in hypothalamus ( 3 H)nisoxetine binding; moreover, plasma adrenocorticotropin-releasing hormone responses to a 5-min open field test were amplified by prior repeated restraint in both strains, but desipramine prevented such an amplification in WKY rats only. However, neither elevated plus-maze nor open field behaviors of SHRs and WKY rats were affected by desipramine pretreatment. Thus, the SHR and WKY rat strains may prove useful in understanding how genetic differences in noradrenergic responses to repeated stress and desipramine treatment impact on adaptive processes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuropharmacology Elsevier

Strain-dependent neurochemical and neuroendocrine effects of desipramine, but not fluoxetine or imipramine, in Spontaneously Hypertensive and Wistar–Kyoto rats

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Publisher
Elsevier
Copyright
Copyright © 2000 Elsevier Science Ltd
ISSN
0028-3908
eISSN
1873-7064
DOI
10.1016/S0028-3908(00)00088-5
Publisher site
See Article on Publisher Site

Abstract

Spontaneously Hypertensive rats (SHRs) and Wistar–Kyoto (WKY) rats differ in their emotional responses to stress and antidepressant administration. We have analysed different neurochemical and psychoneuroendocrine responses to repeated pretreatments with fluoxetine, imipramine or desipramine (10 mg/kg p.o. daily for 4 weeks) in SHRs and WKY rats exposed to a daily 2-h restraint episode for the last 5 days of antidepressant administration. Following a 24-h wash-out period, WKY rats displayed higher plasma antidepressant and antidepressant metabolite levels than SHRs. Fluoxetine pretreatment decreased ( 3 H)citalopram binding at midbrain serotonin (5-HT) transporters, whereas tricyclic and/or fluoxetine decreased ( 3 H)ketanserin binding at cortical 5-HT 2A receptors, ( 3 H)CGP-12177 binding at cortical ß -adrenoceptors, and ( 3 H)nisoxetine binding at midbrain noradrenaline (NA) transporters in both strains. None of the antidepressants affected ( 3 H)8-hydroxy-2-(di- N -propylamino)tetralin binding at hippocampal 5-HT 1A receptors. In WKY rats, repeated restraint triggered a desipramine-sensitive 140% increase in hypothalamus ( 3 H)nisoxetine binding; moreover, plasma adrenocorticotropin-releasing hormone responses to a 5-min open field test were amplified by prior repeated restraint in both strains, but desipramine prevented such an amplification in WKY rats only. However, neither elevated plus-maze nor open field behaviors of SHRs and WKY rats were affected by desipramine pretreatment. Thus, the SHR and WKY rat strains may prove useful in understanding how genetic differences in noradrenergic responses to repeated stress and desipramine treatment impact on adaptive processes.

Journal

NeuropharmacologyElsevier

Published: Nov 1, 2000

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