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J Korean Neurol Assoc. 1995 Jun;13(2):177-186. Korean. In Vitro.
Lee SH , Shin BS , Seo MW , Kim YH , Kim KW .
Department of Neurology, College of Medicine, Chon-Buk University, Korea.
Department of Pharmacology, College of Medicine, Chon-Buk University, Korea.
Abstract

OBJECTIVE & BACKGROUND: It has been shown that cerebral ischemia alters brain monoamine metabolism. In an attempt to elucidate the. Mechanism for ischen-iiainduced release of neurotransmitters in vitro, we examined the ischemia-induced release of (3H) norepinephrine (NE) from cerebral cortex of the rat. RESULTS: Ischemia, deprivation of oxygen and glucose, induced significant (about 12% of total tissue content) release of (3H)NE from cerebral cortex in vitro. This ischemia-induced release of (3H)NE from cerebral cortex was significantly attenuated by 1 mM TTX (tetrodotoxin), 1. 2 mM Mg2+, 10 mM MK-801, 10 mM ketamine, NMDA receptor antagonist, 30 mM DNQX, a kainate/AMPA receptor antagonist, or a 30 mM carbetapentane, an inhibitor of glutarnate release Dantrolene(30 mM) and ryanodine (100 nM), inhibitors of intraceuular Ca2+ release, flunarizine(5 mM) and w-conotoxin (100 nM), inhibitors of N-type Ca2+ channels, significantly attenuated the ischeniiainduced release of (3H)NF, but verapamil (5mM), an inhibitor of L-type Ca2+ channels, did not. Nisoxetine(100 nM), a relative NE transporter blocker, significantly inhibited the ischemia-induced release of (3H) NE. Removal of Ca2+ from the incubation media potently increased ischemia-induced (3H)NE release. CONCLUSION: These results suggest that ischemia-evoked release of norepienphrine was caused by release of glutamate via activation of NMDA and non-NMDA receptors, and that Ca2+-dependent and -independent release processes are underlying in this phenomenon.

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