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pubmed-article:10978576pubmed:abstractTextTo evaluate the involvement of brain protein kinase C (PKC) in the stress-induced activation of hypothalamic-pituitary-adrenal (HPA) axis, we examined the effects of PKC inhibitors administered intracerebroventricularly (i.c.v.) on the immobilization stress-induced plasma corticosterone levels in mice. Calphostin C (a pan-specific PKC inhibitor) injected i.c.v. decreased the immobilization stress-induced plasma corticosterone level: maximal inhibition of 35% was attained at a dose of 100 pmol. Gö 6976 (an alpha and beta1 PKC isotype-selective inhibitor) was less effective than Calphostin C: maximal inhibition of 17% was attained at a dose of 30 pmol. Phorbol 12-myristate 13-acetate (a general PKC activator) injected i.c.v. at doses of 16 and 48 pmol increased the plasma corticosterone levels in a dose-dependent manner. The present study demonstrates the involvement of PKC in the brain in the regulation of the immobilization stress-induced stimulation of HPA axis in vivo.lld:pubmed
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pubmed-article:10978576pubmed:authorpubmed-author:KimY HYHlld:pubmed
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pubmed-article:10978576pubmed:articleTitleInhibition of brain protein kinase C attenuates immobilization stress-induced plasma corticosterone levels in mice.lld:pubmed
pubmed-article:10978576pubmed:affiliationDepartment of Psychiatry, College of Medicine, Hallym University, Chunchon, 200-702, Kangwon-Do, South Korea.lld:pubmed
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