Ashwood T J, Wheal H V
Neurosci Lett. 1986 Jun 18;67(2):147-52. doi: 10.1016/0304-3940(86)90388-5.
Epileptiform bursts of population spikes were evoked in the CA1 region of slices of the hippocampus in which the CA3 region had been previously lesioned with kainic acid. D-2-amino-5-phosphonovalerate (D-APV), a specific N-methyl-D-aspartate (NMDA) antagonist, would markedly reduce the number of spikes in the burst but had no effects on the primary population spike or the amplitude of the field excitatory postsynaptic potential (EPSP). In unlesioned control slices only a single population spike was evoked and D-APV had no effect on this response or the field EPSP. Multiple population spike bursts evoked following application of bicuculline to control slices were much less attenuated by D-APV. The results suggest that activation of NMDA receptors contributes to the production of epileptiform activity in the kainic acid-lesioned hippocampus.
在先前用 kainic 酸损伤了 CA3 区的海马切片的 CA1 区诱发了群体峰电位的癫痫样爆发。D-2-氨基-5-膦酸戊酸（D-APV），一种特异性 N-甲基-D-天冬氨酸（NMDA）拮抗剂，会显著减少爆发中峰电位的数量，但对初级群体峰电位或场兴奋性突触后电位（EPSP）的幅度没有影响。在未损伤的对照切片中，仅诱发了单个群体峰电位，D-APV 对该反应或场 EPSP 没有影响。在对照切片中应用荷包牡丹碱后诱发的多个群体峰电位爆发被 D-APV 减弱的程度要小得多。结果表明，NMDA 受体的激活有助于在 kainic 酸损伤的海马中产生癫痫样活动。
