• Pharmacol. Biochem. Behav. · Jan 2012

    A role for 5-HT1A receptors in the basolateral amygdala in the development of conditioned defeat in Syrian hamsters.

    • Kathleen E Morrison and Matthew A Cooper.
    • Department of Psychology, University of Tennessee, Knoxville, TN 37996-0900, USA. kmcinty1@utk.edu
    • Pharmacol. Biochem. Behav. 2012 Jan 1; 100 (3): 592-600.

    AbstractThe basolateral nucleus of the amygdala (BLA) is a key brain region regulating behavioral changes following stressful events, including social defeat. Previous research has shown that activation of serotonin (5-HT) 1A receptors in the BLA reduces conditioned fear and anxiety-like behavior. The objective of this study was to test whether 5-HT1A receptors in the BLA contribute to conditioned defeat in male Syrian hamsters (Mesocricetus auratus). We tested whether injection of the selective 5-HT1A receptor agonist flesinoxan (400 ng, 800 ng, or 1200 ng in 200 nl saline) into the BLA prior to social defeat would reduce the acquisition of conditioned defeat, and whether a similar injection prior to testing would reduce the expression of conditioned defeat. We also tested whether injection of the selective 5-HT1A receptor antagonist WAY-100635 (400 ng or 1600 ng in 200 nl saline) into the BLA prior to social defeat would enhance the acquisition of conditioned defeat, and whether a similar injection prior to testing would enhance the expression of conditioned defeat. We found that injection of flesinoxan into the BLA decreased both the acquisition and expression of conditioned defeat. However, injection of WAY-100635 into the BLA did not alter the acquisition or expression of conditioned defeat. These data indicate that pharmacological activation of 5-HT1A receptors in the BLA is sufficient to impair the acquisition and expression of conditioned defeat. Our results suggest that pharmacological treatments that activate 5-HT1A receptors in the BLA are capable of reducing the development of stress-induced changes in behavior.Copyright © 2011 Elsevier Inc. All rights reserved.

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