Tsubokawa H, Oguro K, Masuzawa T, Kawai N
Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.
Neurosci Lett. 1995 May 19;191(1-2):95-8. doi: 10.1016/0304-3940(95)11569-4.
The changes in the spontaneous excitatory postsynaptic currents (sEPSCs) after transient cerebral ischemia were studied using whole-cell recording from CA1 pyramidal neurons in the gerbil. In neurons recorded 1-2 days after ischemia, sEPSCs had a slowed time course with the decay time constant fitted by a single exponential and it progressively increased after ischemia. Frequency and amplitude distribution of sEPSCs in ischemic neurons were not significantly different from those in the control neurons. The results support the view that abnormal non-N-methyl-D-aspartic acid currents originate at the degenerated postsynaptic site, unrelated to the presynaptic releasing mechanisms.
利用全细胞膜片钳记录技术，研究了沙土鼠海马CA1区锥体神经元在短暂性脑缺血后自发性兴奋性突触后电流（sEPSCs）的变化。在缺血后1-2天记录的神经元中，sEPSCs的时间进程减慢，其衰减时间常数可用单指数函数拟合，且缺血后逐渐增加。缺血神经元中sEPSCs的频率和幅度分布与对照神经元无显著差异。这些结果支持以下观点：异常的非N-甲基-D-天冬氨酸电流起源于退化的突触后位点，与突触前释放机制无关。
