Ischemia-Induced Release of (3H) norepinephrine from Rat Cerebral Cortex Slices.
- Author:
Sang Hyo LEE
1
;
Byoung Soo SHIN
;
Man Wook SEO
;
Young Hyum KIM
;
Kee Won KIM
Author Information
1. Department of Neurology, College of Medicine, Chon-Buk University, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Cerebral ischemia;
glutamate;
norepinephrine;
Ca2+;
cerebral cortex
- MeSH:
Animals;
Brain;
Brain Ischemia;
Cerebral Cortex*;
Dizocilpine Maleate;
Glucose;
Glutamic Acid;
Ischemia;
Ketamine;
Metabolism;
N-Methylaspartate;
Neurotransmitter Agents;
Norepinephrine*;
Oxygen;
Rats*;
Ryanodine;
Verapamil
- From:Journal of the Korean Neurological Association
1995;13(2):177-186
- CountryRepublic of Korea
- Language:Korean
-
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.
