INHIBITORY SYNAPTIC CURRENTS IN STELLATE CELLS OF RAT CEREBELLAR SLICES
INHIBITORY SYNAPTIC CURRENTS IN STELLATE CELLS OF RAT CEREBELLAR SLICES
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DOI：
10.1113/jphysiol.1993.sp019766
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发表时间：
1993-08-01
影响因子：
5.5
通讯作者：
GERSCHENFELD, HM
中科院分区：
文献类型：
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作者：
LLANO, I;GERSCHENFELD, HM
1.在14-21日龄的大鼠小脑薄片上，采用密封全细胞记录技术研究了位于分子层外三分之二的星状细胞（8-9 μ m索马直径）的电压门控电流、突触电流和GABA反应.在对称Cl-条件下，电压钳位在-60 mV的星状细胞显示自发的抑制性突触后电流（IPSC）。与相同细胞的GABA（A）反应一样，IPSC被荷包牡丹碱阻断。IPSC的发生频率范围为每秒0.2至1.9起事件（21个细胞）。事件的平均振幅范围为61至226 pA（平均值+/- S.E.M.：132 +/-11; n = 21）。IPSC的时间进程的特点是快速上升（平均值± S。E. M.达到峰值的时间：1.1 +/-0.1ms，n = 7）和缓慢衰减。衰减阶段由双指数函数描述，时间常数分别为8.7 ± 0-6 ms和40.9 ± 3.7 ms（平均值± S.E.M.; n = 7）。在对照盐水中记录的自发突触事件的一小部分（15至20%）具有比IPSC更快的起始，并且以快速单指数衰减（时间常数为1.0-1.3 ms）衰减。这些是兴奋性突触后电流（EPSC），不受荷包牡丹碱的影响，并被谷氨酸受体拮抗剂6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX）阻断。TTX（0.5-1 μ m）的浴涂可阻断星状细胞中的电压门控Na+电流，诱导IPSC频率的可变降低（平均值± S.E.M.; TTX与对照组的频率比：0.47 +/- 0.09; n = 12）。然而，毒素对1 PSC的平均振幅或动力学没有显著影响。微型IPSC的平均振幅为141 +/-13pA（平均+/- S.E.M.; n = 22）。在含TTX的溶液中，当通过去除细胞外Ca 2+和添加EGTA或通过添加Cd 2+消除Ca“电流时，IPSC的频率不受影响。200-300 pA的微型IPSC仍被保留。在对称的Cl-条件下，局部应用GABA的星状细胞诱导的内向电流和膜噪声的增加。响应GABA的长期应用表现出脱敏在全细胞模式和体细胞外补丁。弦电导估计记录单个GABA通道事件在体细胞外向补丁是28 pS.8。目前的结果表明，在星状细胞中，单个量子递质的释放激活了大量的突触后GABA（A）受体门控通道。
1. In thin cerebellar slices of rats aged 14-21 days, voltage-gated currents, synaptic currents and GABA responses were studied with the tight-seal whole-cell recording technique from stellate cells (8-9 mum soma diameter) located in the outer two-thirds of the molecular layer.2. In symmetrical Cl- conditions, stellate cells voltage-clamped at -60 mV showed spontaneous inhibitory postsynaptic currents (IPSCs). As were the GABA(A) responses of the same cells, the IPSCs were blocked by bicuculline. The frequency of occurrence of IPSCs ranged from 0.2 to 1.9 events per second (21 cells). The mean amplitude of the events ranged from 61 to 226 pA (mean +/- S.E.M.: 132 +/-11; n = 21).3. The temporal course of IPSCs was characterized by a rapid rise (mean + S. E. M. of the time to peak: 1.1 +/- 0.1 ms, n = 7) and a slow decay. The decay phase was described by a double exponential function with time constants of 8.7 +/- 0-6 ms, and 40.9 + 3.7 ms respectively (means + S.E.M.; n = 7).4. A minor fraction (15 to 20%) of the spontaneous synaptic events recorded in control saline had a faster onset than that of the IPSCs and decayed with a rapid mono-exponential decay (time constant of 1.0-1.3 ms). These were excitatory postsynaptic currents (EPSCs) unaffected by bicuculline and blocked by the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX).5. Bath application of TTX (0.5-1 mum), which blocked voltage-gated Na+ currents in stellate cells, induced a variable decrease in the frequency of IPSCs (mean + S.E.M.; of the frequency ratio in TTX over control: 0.47 +/- 0.09; n = 12). However, the toxin had no significant effect either on the mean amplitude or on the kinetics of the 1PSCs. The mean amplitude of the miniature IPSCs was 141 +/- 13pA (mean +/- S.E.M.; n = 22).6. In TTX-containing solutions, the frequency of the IPSCs was unaffected when Ca'' currents were eliminated either by removal of extracellular Ca2+ and addition of EGTA, or by addition of Cd2+. Miniature IPSCs of 200-300 pA were still observed.7. In symmetrical Cl- conditions, local application of GABA to stellate cells induced an inward current and an increase in membrane noise. Responses to prolonged applications of GABA showed desensitization in both whole-cell mode and somatic outside-out patches. The chord conductance estimated from recording single GABA channel events in somatic outside-out patches was 28 pS.8. The present results suggest that in stellate cells the release of a single quantum of transmitter activates a large number of postsynaptic GABA(A) receptor-gated channels.