Studies have shown that intracerebroventricular (i.c.v.) injection (10-20-mu-g) of corticotropin releasing factor (CRF) in rats induces epileptiform activity characterized by a regular (pacemaker-like) spiking pattern located in hippocampal leads. CRF has also been shown to increase the firing rate of noradrenergic neurons in the locus ceruleus. Our experiments clarified the possible role of norepinephrine (NE) in mediating hippocampal activity of CRF. Intraperitoneal (i.p.) injection of the alpha-2-agonist clonidine at a dose of 0.5-5-mu-g/kg prevented, in a dose-related manner, the hippocampal epileptiform activity induced by CRF (20-mu-g i.c.v.). Our results suggest a possible role of NE in CRF-induced spiking activity.
CLONIDINE PREVENTS CORTICOTROPIN RELEASING FACTOR-INDUCED EPILEPTOGENIC ACTIVITY IN RATS
MARROSU, FRANCESCO;FRATTA, WALTER
1992-01-01
Abstract
Studies have shown that intracerebroventricular (i.c.v.) injection (10-20-mu-g) of corticotropin releasing factor (CRF) in rats induces epileptiform activity characterized by a regular (pacemaker-like) spiking pattern located in hippocampal leads. CRF has also been shown to increase the firing rate of noradrenergic neurons in the locus ceruleus. Our experiments clarified the possible role of norepinephrine (NE) in mediating hippocampal activity of CRF. Intraperitoneal (i.p.) injection of the alpha-2-agonist clonidine at a dose of 0.5-5-mu-g/kg prevented, in a dose-related manner, the hippocampal epileptiform activity induced by CRF (20-mu-g i.c.v.). Our results suggest a possible role of NE in CRF-induced spiking activity.
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