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Abstract
Introduction of a socially naive male rat into the home territory of a resident counterpart
results in agonistic interactions, leading to the rapid social defeat of the intruder.
Exposure to the aggressive resident produces a stress-response profile consisting
of neuroendocrine activation and coping behaviors such as submission. The present
studies examined the dependence of these adaptive responses on endogenous brain Corticotropin-Releasing
Factor (CRF), a peptide hormone known to coordinate neuronally mediated- and pituitary-adrenal
responses to stress. The Elevated Plus-Maze was employed as an animal model of emotionality
in which stressors reduce subsequent exploration of open maze arms without walls in
favor of enclosed maze arms. A CRF antagonist, alpha-hel CRF9-41, administered intracerebroventricularly
(5 and 25 micrograms i.c.v.) immediately post-stress and 5 min prior to maze testing
reversed the heightened emotionality produced by the resident exposure stressor. This
action paralleled that of an anxiolytic dose of the short-acting benzodiazepine, midazolam
(1.5 mg/kg i.p.). Intra-amygdaloid administration of lower doses of the CRF antagonist
(125, 250 and 500 ng i.c.) also reversed, dose-dependently, the effect of exposure
to an aggressive resident without altering the behavior of unstressed control animals.
Further, the enhanced release of ACTH and corticosterone following social conflict
was not modified over the short term by the intra-amygdaloid dose of CRF antagonist
(250 ng i.c.) which was effective in reversing stress-induced hyper-emotionality.
These results suggest that limbic system CRF substrates exert an anxiogenic effect
on the exploratory behavior of socially defeated rats via a pituitary-adrenal-independent
mechanism.