双侧黑质内注入N-甲基-D-天冬氨酸可抑制神经元损伤，且不影响大鼠中 kainic 酸诱导的癫痫发作持续时间。

Bilateral intranigral NMDA infusion suppresses neuronal injury without affecting the duration of kainic acid-induced seizures in rats.

作者信息

Tanaka K, Henshall D C, Waga S, Shimosaka S, Simon R P

机构信息

Department of Neurology, University of Pittsburgh, PA 15213, USA.

出版信息

Neurosci Lett. 1998 Jul 17;251(1):69-71. doi: 10.1016/s0304-3940(98)00483-2.

DOI:10.1016/s0304-3940(98)00483-2

PMID:9714467

Abstract

The substantia nigra pars reticulata (SNpr) is recognized as an important modulator of seizures within the limbic system. We have investigated the effects of N-methyl-D-aspartate (NMDA) infusion into SNpr upon seizure-related neuronal injury (assessed by expression of the 72-kDa heat shock protein - HSP 72) induced by systemic kainic acid (KA) in rats. Three to four days following implantation of guide cannulae for drug administration into SNpr, KA (7 mg/kg) was injected intravenously to induce seizures. Bilateral intranigral infusion of NMDA (20 nmol) 15 min prior to KA injection, suppressed the expression of HSP 72 in the hippocampal CA1 region without affecting seizure duration. These results support the involvement of NMDA receptors within SNpr in modulating neuronal injury following KA-induced limbic seizures.

摘要

黑质网状部（SNpr）被认为是边缘系统内癫痫发作的重要调节因子。我们研究了向大鼠SNpr内注入N-甲基-D-天冬氨酸（NMDA）对全身性海藻酸（KA）诱导的癫痫相关神经元损伤（通过72-kDa热休克蛋白 - HSP 72的表达评估）的影响。在将给药引导套管植入SNpr三到四天后，静脉注射KA（7 mg/kg）以诱导癫痫发作。在KA注射前15分钟双侧黑质内注入NMDA（20 nmol），可抑制海马CA1区HSP 72的表达，而不影响癫痫发作持续时间。这些结果支持SNpr内的NMDA受体参与调节KA诱导的边缘性癫痫发作后的神经元损伤。