Immunohistochemical studies of noradrenergic-induced expression of c-fos in the rat CNS.
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.
Department of Psychiatry, New York University School of Medicine, NY 10016.
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Bing
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Stone
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Zhang
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D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D015153:Blotting, Western; D001921:Brain / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D007093:Imidazoles; D016760:Proto-Oncogene Proteins c-fos; C050701:atipamezole; D015016:Yohimbine; D009638:Norepinephrine