Herron C E, Williamson R, Collingridge G L
Neurosci Lett. 1985 Nov 11;61(3):255-60. doi: 10.1016/0304-3940(85)90473-2.
The sensitivity of convulsant-induced epileptiform activity in the hippocampus to the selective N-methyl-D-aspartate (NMDA) antagonist D-2-amino-5-phosphonovalerate (D-APV) was examined using in vitro electrophysiological techniques. This compound reduced the number and size of the synaptically evoked population spikes recorded in the CA1 region in the presence of the convulsants, pentylenetetrazol, bicuculline or folate. Intracellular recordings in the presence of bicuculline showed that D-APV reduced the late component of the excitatory postsynaptic potential and the number of action potentials evoked synaptically. A mechanism is suggested to explain how NMDA receptors, which are known not to be involved in normal synaptic transmission in hippocampal slices, can contribute to epileptiform activity.
运用体外电生理技术，研究了惊厥诱导的海马癫痫样活动对选择性N-甲基-D-天冬氨酸（NMDA）拮抗剂D-2-氨基-5-磷酸戊酸（D-APV）的敏感性。在惊厥剂戊四氮、荷包牡丹碱或叶酸存在的情况下，该化合物减少了在CA1区记录到的突触诱发群体峰电位的数量和大小。在荷包牡丹碱存在的情况下进行的细胞内记录表明，D-APV减少了兴奋性突触后电位的晚期成分以及突触诱发的动作电位数量。本文提出了一种机制来解释已知不参与海马切片正常突触传递的NMDA受体如何导致癫痫样活动。
