N-甲基-D-天冬氨酸受体阻滞剂对缺镁大鼠白噪声诱发癫痫预防作用的体内评估

In vivo assessment of prevention of white-noise-induced seizure in magnesium-deficient rats by N-methyl-D-aspartate receptor blockers.

作者信息

Nakamura M, Abe S, Goto Y, Chishaki A, Akazawa K, Kato M

机构信息

Department of Clinical Nutrition, Graduate School of Health and Nutrition Sciences, Nakamura-gakuen College, Fukuoka, Japan.

出版信息

Epilepsy Res. 1994 Mar;17(3):249-56. doi: 10.1016/0920-1211(94)90055-8.

DOI:10.1016/0920-1211(94)90055-8

PMID:8013447

Abstract

The behavioral changes associated with seizures induced by auditory stimulation in magnesium (Mg)-deficient rats originate in deep brain structures and secondarily project to neocortex. In the present study, we examined the roles of N-methyl-D-aspartate (NMDA) receptors in this seizure model. The intraperitoneal administration of the competitive NMDA receptor blocker DL-2-amino-7-phosphonoheptanoic acid (36 and 72 mg/kg) and the non-competitive NMDA receptor blocker MK-801 (1.35 and 2.7 mg/kg), completely prevented the induction of seizure and bradyarrhythmia or sudden death resulting from seizure. Therefore, the white-noise-induced seizures in Mg-deficient rats are linked to increased neuronal excitability via the NMDA receptor.

摘要

镁缺乏大鼠因听觉刺激诱发癫痫发作所伴随的行为变化起源于深部脑结构，继而投射至新皮质。在本研究中，我们考察了N-甲基-D-天冬氨酸（NMDA）受体在该癫痫模型中的作用。腹腔注射竞争性NMDA受体阻断剂DL-2-氨基-7-磷酸庚酸（36和72 mg/kg）以及非竞争性NMDA受体阻断剂MK-801（1.35和2.7 mg/kg），可完全防止癫痫发作以及癫痫发作导致的心律失常或猝死。因此，镁缺乏大鼠中白噪声诱发的癫痫发作与通过NMDA受体增加的神经元兴奋性有关。