Hegstad E, Langmoen I A, Hablitz J J
Department of Neurosurgery, Rikshospitalet, Oslo, Norway.
Epilepsy Res. 1989 Mar-Apr;3(2):174-7. doi: 10.1016/0920-1211(89)90046-6.
Exposure of neocortical slices from immature rats to saline containing no added magnesium induced spontaneous epileptiform activity that consisted of bursts of low-amplitude isolated discharges lasting 50-90 sec, recurring every 90-300 sec. Bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-7-phosphonoheptanoic acid led to a rapid, reversible suppression of epileptiform activity, indicating involvement of NMDA receptors. Perfusion with zinc or glycine, putative modulators of the NMDA receptor, with suppressive and enhancing properties, respectively, had no effect on the frequency or duration of the epileptiform discharges. These results indicate that in the immature neocortex in vitro, application of zinc or glycine does not modulate NMDA receptor-mediated, low-magnesium-induced epileptiform discharges.
将未成熟大鼠的新皮质切片暴露于未添加镁的盐溶液中,会诱发自发性癫痫样活动,其由持续50 - 90秒的低幅孤立放电爆发组成,每90 - 300秒重复一次。浴用N - 甲基 - D - 天冬氨酸(NMDA)受体拮抗剂DL - 2 - 氨基 - 7 - 膦酰庚酸会导致癫痫样活动迅速、可逆地受到抑制,表明NMDA受体参与其中。分别用锌或甘氨酸灌注,它们分别是具有抑制和增强特性的NMDA受体假定调节剂,对癫痫样放电的频率或持续时间没有影响。这些结果表明,在体外未成熟的新皮质中,应用锌或甘氨酸不会调节NMDA受体介导的、低镁诱导的癫痫样放电。