Study on the 3HAcetylcholine Release Induced by Oxygen-Glucose Deprivation in Rat Cerebral Cortical Slices.
- Author:
Jeong Ju LEE
1
;
Kee Won KIM
;
Man Wook SEO
;
Young Hyun KIM
Author Information
1. Department of Neurology, Medical School, Chonbuk National University.
- Publication Type:In Vitro ; Original Article
- Keywords:
[3H]Ach release;
cerebral cortical slices;
ischemia
- MeSH:
6-Cyano-7-nitroquinoxaline-2,3-dione;
Acetylcholine;
Animals;
Brain;
Brain Ischemia;
Calcium;
Dantrolene;
Dizocilpine Maleate;
Ischemia;
Ketamine;
Metabolism;
N-Methylaspartate;
Nimodipine;
Nitrendipine;
Oxygen;
Rats*;
Receptors, AMPA;
Suspensions;
Synaptic Transmission;
Tetrodotoxin
- From:Journal of the Korean Neurological Association
1998;16(4):530-535
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: It has been shown that cerebral ischemia alters brain acetylcholine (Ach) metabolism. In an attempt to elucidate the mechanisms for ischemia-induced release of Ach in vitro, the effects of drugs which can influence the cholinergic neurotransmission on the ischemia-induced release of [3H]Ach from cerebral cortical slices of the rat were examined. METHODS: The cortices of decapitated rats were chopped and dispersed in artificial CSF. Then, the tissue suspensions were incubated with [3H]choline. The tissues were transferred and incubated in washing, hypoglycemic (deprivation of glucose), ischemic (deprivation of oxygen and glucose) and extracting plates sequently. Ischemia-induced release of [3H]Ach was expressed as percentage of the total [3H]Ach present in the slices. RESULTS: Ischemia induced significant release (about 9.3% of total tissue content) of [3H]Ach from cerebral cortical slices in vitro. This [3H]Ach release was significantly attenuated by tetrodotoxin, a voltage-sensitive Na+-channel blocker, and Mg2+, a physiological N-methyl-D-aspartate (NMDA) receptor blocker. Vesamicol (1 M), a blocker of vesicular transport of Ach, MK-801 and ketamine, NMDA receptor antagonists, 6,7-nitroquinoxaline-2,3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), kainate/AMPA receptor antagonists, and 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione (NBQX), a AMPA receptor blocker attenuated the [3H]Ach. Nitrendipine, nimodipine, inhibitor of L-type Ca2+ channels, and -conotoxin GVIA, an inhibitor of N-type Ca2+ channels, significantly attenuated the ischemia-induced release of [3H]Ach. Omission of Ca2+ from incubation media attenuated the ischemia-induced [3H]Ach release. Inhibitors of intracellular Ca2+ release, dantrolene and TMB-8, and a cell-permeable calcium chelator, 1,2-bis (2-aminophenoxy)-ethane-N, N, N+, N+-tetraacetic acid tetrakis (acetoxymethyl) ester (BAPTA-AM), inhibited the ischemia-evoked [3H]Ach release. CONCLUSION: These results suggest that the ischemia can induce Ach rele.
