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F Spiga, Henry Wellcome LINE, University of Bristol, Bristol, BS1 3NY, United Kingdom
L Harrison, Henry Wellcome LINE, University of Bristol, Bristol, United Kingdom
C MacSweeney, Pharmacology, Schering-Plough Corporation, North Lanarkshire, United Kingdom
F Thomson, Molecular Pharmacology, Schering-Plough Corporation, Newhouse, United Kingdom
M Craighead, Molecular Pharmacology, Schering-Plough Corporation, North Lanarkshire, United Kingdom
S Lightman, University of Bristol, Bristol, United Kingdom

Correspondence: Francesca Spiga, Email: F.Spiga{at}bristol.ac.uk

Abstract

Exposure to chronic restraint modifies the hypothalamic-pituitary-adrenal (HPA) axis response to subsequent acute stressors with adaptation of the response to a homotypic and sensitization of the response to a heterotypic stressor. Since vasopressin activity has been reported to change during chronic stress, we investigated whether this was an important factor in HPA facilitation. We therefore tested whether vasopressin 1b receptor (V1bR) blockade altered the ACTH and corticosterone response to heterotypic stressors following chronic restraint stress.

Adult male rats were exposed to chronic restraint (CR), single restraint (SR) or were left undisturbed in the home cage (HCC). Twenty four hours after the last restraint, rats were injected with either a V1b R antagonist (Org, 30 mg/kg, s.c.) or vehicle (5% mulgofen in saline, 0.2/kg, s.c.) and then exposed to either restraint, lipopolysaccharide (LPS) or white noise.

Chronic restraint resulted in the adaptation of the ACTH and corticosterone response to restraint and this effect was not prevented by pre-treatment with Org. Although we found no effect of chronic restraint on LPS-induced ACTH and corticosterone secretion both repeated and single episodes of restraint induced sensitization of the ACTH, but not corticosterone response to acute noise. Pre-treatment with Org was able to reduce the exaggerated ACTH response to noise after both single and repeated exposure to restraint.

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