Patch-Clamp Analysis on the Mechanism for Inhibitory Synaptic Transmission in Rat Spinal Motoneurone.

用全细胞密封法记录新生大鼠脊髓运动神经元抑制性突触后电流(IPSCs)。IPSCs是通过细胞外刺激单个内脏神经元而被激活的。在不同频率(0.2-50 Hz)刺激下，从刺激伪影到IPSCs起始的潜伏期是稳定的，平均潜伏期为0.6-0.8ms(37℃)，提示IPSCs具有单突触的性质。当外加钙离子浓度([Ca]o)降低时，IPSCs的失效次数增加，平均波幅降低。[Ca]o(0.35~1.4 mm)与IPSCs的平均波幅呈线性关系，在双对数坐标系下的平均斜率为3.1。IPSCs的波幅随[Ca]o的降低而降低，但在0.7 mm[Ca]o以下，观察到的IPSCs的波幅(不包括故障)达到一个稳定的“最小”水平。在0.5 mM[Ca]_o中测得的最小IPSCs的平均电导为650ps，与河豚毒素作用下的运动神经元记录的自发微型IPSCs的电导相当。结果表明，在低[Ca]_o下观察到的‘最小’IPSCs可能代表量子IPSCs。量子IPSCs的平均变异系数为0.50。不同运动神经元之间量子IPSCs的平均幅度相差3倍。量子IPSCs的上升时间与其幅度之间没有相关性，表明量子大小的分散不是由于释放部位的不同而引起的。IPSC的统计性质表明，IPSC的幅度不能用二项分布来拟合。结论：新生大鼠脊髓单个抑制性突触中IPSCs的量子大小可能并不一致。

Tight-seal whole-cell recordings of Inhibitory Postsynaptic Currents (IPSCs) were made from neonatal rat spinal motoneurones. The IPSCs were evoked by stimulating a single internuncial neurone extracellularly. The latency measured from the stimulus artifact to the onset of IPSCs was stable when stimulated at various frequencies (0.2-50 Hz) with the mean latency of 0.6-0.8 ms at 37 C, suggesting the monosynaptic nature of the IPSCs. When the external Ca^<2+> concentration ([Ca]_o) was reduced, the number of failures of IPSCs increased, and the mean amplitude of IPSCs decreased. The relation between [Ca]_o (0.35-1.4mM) and the mean amplitude of IPSCs was linear with a mean slope of 3.1 on double logarithmic co-ordinates. The amplitude of IPSCs decreased with a decrease in [Ca]_o. However, below 0.7 mM [Ca]_o, the amplitude of observed IPSCs (excluding failures) reached a steady 'minimum' level. The meah conductance of the 'minimum' IPSCs measured in 0.5 mM [Ca]_o was 650 pS, which was comparable to the conductance of spontaneous miniature IPSCs recorded from motoneurones under tetrodotoxin. It is suggested that the 'minimum' IPSCs observed at low [Ca]_o may represent the quantal IPSCs. The quantal IPSCs had a coefficient of variation of 0.50 on average. The mean amplitude of quantal IPSCs varied among different motoneuromes by a factor of 3. No correlation was observed between the rise time and amplitude of quantal IPSCs, indicating that the dispersion in quantal size is not due to different locations of release sites. The statistical nature of the IPSCs indicated that the amplitude of IPSCs cannot be fitted with a binomial distribution. It is concluded that the quantal size constututing IPSCs may not be uniform at individual inhibitory synapses of neonatal rat spinal cord.