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Title: Rat epileptic seizures evoked by BmK {alpha}IV and its possible mechanisms involved in sodium channels

Abstract

This study showed that rat unilateral intracerebroventricular injection of BmK {alpha}IV, a sodium channel modulator derived from scorpion Buthus martensi Karsch, induced clusters of spikes, epileptic discharges and convulsion-related behavioral changes. BmK {alpha}IV potently promoted the release of endogenous glutamate from rat cerebrocortical synaptosomes. In vitro examination of the effect of BmK {alpha}IV on intrasynaptosomal free calcium concentration [Ca{sup 2+}]{sub i} and sodium concentration [Na{sup +}]{sub i} revealed that BmK {alpha}IV-evoked glutamate release from synaptosomes was associated with an increase in Ca{sup 2+} and Na{sup +} influx. Moreover, BmK {alpha}IV-mediated glutamate release and ion influx was completely blocked by tetrodotoxin, a blocker of sodium channel. Together, these results suggest that the induction of BmK {alpha}IV-evoked epileptic seizures may be involved in the modulation of BmK {alpha}IV on tetrodotoxin-sensitive sodium channels located on the nerve terminal, which subsequently enhances the Ca{sup 2+} influx to cause an increase of glutamate release. These findings may provide some insight regarding the mechanism of neuronal action of BmK {alpha}IV in the central nervous system for understanding epileptogenesis involved in sodium channels.

Authors:
 [1];  [1];  [1];  [2];  [1];  [3];  [4]
  1. Graduate School of the Chinese Academy of Sciences, Shanghai Institute of Physiology, Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031 (China)
  2. (United States)
  3. School of Life Sciences of Shanghai University, Shang-Da Road 99, Shanghai 200444 (China)
  4. School of Life Sciences of Shanghai University, Shang-Da Road 99, Shanghai 200444 (China). E-mail: yhji@server.shcnc.ac.cn
Publication Date:
OSTI Identifier:
20976914
Resource Type:
Journal Article
Resource Relation:
Journal Name: Toxicology and Applied Pharmacology; Journal Volume: 220; Journal Issue: 3; Other Information: DOI: 10.1016/j.taap.2007.01.006; PII: S0041-008X(07)00022-1; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; CALCIUM; CALCIUM IONS; CENTRAL NERVOUS SYSTEM; IN VITRO; INDUCTION; INJECTION; MODULATION; RATS; SCORPIONS; SODIUM; SODIUM IONS

Citation Formats

Chai Zhifang, Bai Zhantao, Zhang Xuying, Membrane Signaling Group, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, Liu Tong, Pang Xueyan, and Ji Yonghua. Rat epileptic seizures evoked by BmK {alpha}IV and its possible mechanisms involved in sodium channels. United States: N. p., 2007. Web. doi:10.1016/j.taap.2007.01.006.
Chai Zhifang, Bai Zhantao, Zhang Xuying, Membrane Signaling Group, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, Liu Tong, Pang Xueyan, & Ji Yonghua. Rat epileptic seizures evoked by BmK {alpha}IV and its possible mechanisms involved in sodium channels. United States. doi:10.1016/j.taap.2007.01.006.
Chai Zhifang, Bai Zhantao, Zhang Xuying, Membrane Signaling Group, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, Liu Tong, Pang Xueyan, and Ji Yonghua. Tue . "Rat epileptic seizures evoked by BmK {alpha}IV and its possible mechanisms involved in sodium channels". United States. doi:10.1016/j.taap.2007.01.006.
@article{osti_20976914,
title = {Rat epileptic seizures evoked by BmK {alpha}IV and its possible mechanisms involved in sodium channels},
author = {Chai Zhifang and Bai Zhantao and Zhang Xuying and Membrane Signaling Group, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709 and Liu Tong and Pang Xueyan and Ji Yonghua},
abstractNote = {This study showed that rat unilateral intracerebroventricular injection of BmK {alpha}IV, a sodium channel modulator derived from scorpion Buthus martensi Karsch, induced clusters of spikes, epileptic discharges and convulsion-related behavioral changes. BmK {alpha}IV potently promoted the release of endogenous glutamate from rat cerebrocortical synaptosomes. In vitro examination of the effect of BmK {alpha}IV on intrasynaptosomal free calcium concentration [Ca{sup 2+}]{sub i} and sodium concentration [Na{sup +}]{sub i} revealed that BmK {alpha}IV-evoked glutamate release from synaptosomes was associated with an increase in Ca{sup 2+} and Na{sup +} influx. Moreover, BmK {alpha}IV-mediated glutamate release and ion influx was completely blocked by tetrodotoxin, a blocker of sodium channel. Together, these results suggest that the induction of BmK {alpha}IV-evoked epileptic seizures may be involved in the modulation of BmK {alpha}IV on tetrodotoxin-sensitive sodium channels located on the nerve terminal, which subsequently enhances the Ca{sup 2+} influx to cause an increase of glutamate release. These findings may provide some insight regarding the mechanism of neuronal action of BmK {alpha}IV in the central nervous system for understanding epileptogenesis involved in sodium channels.},
doi = {10.1016/j.taap.2007.01.006},
journal = {Toxicology and Applied Pharmacology},
number = 3,
volume = 220,
place = {United States},
year = {Tue May 01 00:00:00 EDT 2007},
month = {Tue May 01 00:00:00 EDT 2007}
}