Immunohistochemical studies of noradrenergic-induced expression of c- fos in the rat CNS

Abstract

Previous studies have shown that stimulation of adrenergic receptors in the rat brain causes increased levels of mRNA of the immediate early gene, c- fos. The present studies were undertaken to determine if this stimulation also induces increased levels of c- fos immunoreactivity in the central nervous system (CNS). Rats were treated with the alpha-2 adrenoceptor blockers, yohimbine or atipamezole, or with restraint stress to activate central noradrenergic activity and were perfused 2 h later for immunohistochemical analysis of the cerebral cortex. Yohimbine, atipamezole and restraint stress each was found to cause increases in c- fos-like immunoreactivity (c- fos-li). Western blot analysis revealed increased c- fos protein in the cortex after yohimbine treatment. The c- fos-li response to yohimbine was blocked by prior administration of the beta receptor antagonist, dl-propranolol, and to a lesser degree by the alpha-1 antagonist, prazosin. It is concluded that adrenergic receptor stimulation in the cortex causes increased production of c- fos or fos related antigens and that this (these) immediate early gene product(s) may play a role in noradrenergic function in the CNS.