Voltage clamp analysis of excitatory synaptic transmission in the avian nucleus magnocellularis.
Voltage clamp analysis of excitatory synaptic transmission in the avian nucleus magnocellularis.
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鸟类大细胞核兴奋性突触传递的电压钳分析。
DOI：
10.1113/jphysiol.1994.sp020346
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Trussell,LO
中科院分区：
文献类型：
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作者：
Zhang,S;Trussell,LO
1. 诱发性兴奋性突触后电流 (EPSC) 和自发性微型兴奋性突触后电流 (mEPSC) 的特性已在大细胞核 (nMAG) 的神经元中进行了研究，大细胞核是鸟类耳蜗核之一，接受听觉神经纤维的体细胞、萼神经支配。全细胞膜片钳技术用于对脑切片中视觉识别的神经元进行电压钳位。 2. 在 ‐25 mV 的驱动力下，单个轴突输入激活产生的 EPSC 平均为 ‐5.3 nA。 EPSC 峰值的电流-电压关系与 211 nS 的峰值电导呈线性关系。 EPSC衰减速率随温度呈线性增加，25℃至35℃温度系数（Q10）为2.2；在体内（41 摄氏度），EPSC 将在 0.2 毫秒内衰减。 3. EPSC 由两种药理学和动力学上不同的成分组成：由非 NMDA（N-甲基-D-天冬氨酸）受体引起的早期阶段和由 NMDA 受体引起的晚期阶段。两个分量都在 0 mV 附近反转。虽然谷氨酸受体的两种亚型均被递质激活，但 NMDA 受体在正电势下具有峰值电导，仅为非 NMDA 受体成分峰值的 11%。 4. EPSC 在一系列刺激期间表现出幅度逐渐减小。抑郁程度随着刺激频率的增加而增加，并通过防止受体脱敏的药物而减少，这表明突触后因素在一定程度上限制了重复突触活动期间的突触强度。此外，EPSC 振幅的变异系数在训练过程中增加，与突触前抑制一致。 5. mEPSC 在河豚毒素存在的情况下随机发生，并且可能对应于递质量子。这些突触事件在 100 微秒内上升 (10-90%)，并在 29-32 摄氏度下以 180 微秒的指数衰减。尽管突触位于体细胞位置，mEPSC 的幅度变化很大，表明每个突触位点的量子突触电流存在差异。 EPSC 和 mEPSC 的平均峰值电导之比给出的估计量子含量为 103。
1. The properties of evoked excitatory postsynaptic currents (EPSCs) and spontaneous miniature excitatory postsynaptic currents (mEPSCs) have been studied in neurons of the nucleus magnocellularis (nMAG), one of the avian cochlear nuclei which receive somatic, calyceal innervation from auditory nerve fibres. Whole‐cell patch clamp techniques were used to voltage clamp visually identified neurons in brain slices. 2. EPSCs resulting from activation of single axonal inputs were on average ‐5.3 nA at a driving force of ‐25 mV. Current‐voltage relationships for the peak of the EPSC were linear with a peak conductance of 211 nS. The rate of EPSC decay showed a linear increase with temperature, with a temperature coefficient (Q10) of 2.2 between 25 and 35 degrees C; in vivo (41 degrees C) the EPSC would decay in 0.2 ms. 3. The EPSC was composed of two pharmacologically and kinetically distinct components: an early phase due to non‐NMDA (N‐methyl‐D‐aspartate) receptors and a late phase resulting from NMDA receptors. Both components reversed near 0 mV. While both subtypes of glutamate receptor were activated by transmitter, NMDA receptors had a peak conductance at positive potentials which was only 11% of the peak non‐NMDA receptor component. 4. EPSCs during trains of stimuli exhibited a progressive decrease in amplitude. The extent of depression increased with the frequency of stimulation and was reduced by drugs which prevent receptor desensitization, indicating that, in part, postsynaptic factors limit synaptic strength during repetitive synaptic activity. Additionally, the coefficient of variation of the EPSC amplitude increased during trains, consistent with presynaptic depression. 5. mEPSCs occurred randomly in the presence of tetrodotoxin and presumably correspond to transmitter quanta. These synaptic events rose (10‐90%) within 100 microseconds and decayed with an exponential of 180 microseconds at 29‐32 degrees C. Despite the somatic location of the synapse, mEPSCs varied widely in amplitude, suggesting differences in the quantal synaptic current at each synaptic site. The ratio of the average peak conductance of the EPSC and mEPSC gave an estimated quantal content of 103.