Lee W L, Hablitz J J
Neurobiology Research Center, University of Alabama, Birmingham 35294.
Neurosci Lett. 1989 Dec 15;107(1-3):129-34. doi: 10.1016/0304-3940(89)90804-5.
The ability of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to suppress picrotoxin-induced epileptiform burst activity was examined. Intracellular recordings were obtained from hippocampal CA1 and CA3 pyramidal neurons maintained in vitro. Bath application of CNQX (5 microM) significantly reduced or abolished evoked paroxysmal depolarizing shifts (PDSs) in all CA1 and CA3 neurons tested. In cells where a CNQX-insensitive component in the PDS was manifest, this remaining activity was abolished by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (20 microM), suggesting the existence of a NMDA-mediated synaptic potential. Our results indicate that non-NMDA receptor antagonists are capable of markedly reducing picrotoxin-induced epileptiform activity and that these receptors play an important role in generation of PDSs.
研究了非NMDA受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）抑制印防己毒素诱导的癫痫样爆发活动的能力。从体外培养的海马CA1和CA3锥体神经元进行细胞内记录。浴用CNQX（5微摩尔）显著降低或消除了所有测试的CA1和CA3神经元中诱发的阵发性去极化偏移（PDSs）。在PDS中表现出对CNQX不敏感成分的细胞中，这种剩余活动被N-甲基-D-天冬氨酸（NMDA）受体拮抗剂D-2-氨基-5-磷酸戊酸（20微摩尔）消除，提示存在NMDA介导的突触电位。我们的结果表明，非NMDA受体拮抗剂能够显著降低印防己毒素诱导的癫痫样活动，并且这些受体在PDS的产生中起重要作用。
