Titz S, Keller B U
Zentrum Physiologie und Pathophysiologie, Universität Göttingen, Germany.
J Neurophysiol. 1997 Jul;78(1):82-91. doi: 10.1152/jn.1997.78.1.82.
Excitatory synaptic transmission was investigated in interneurons of the parvocellular nucleus tractus solitarius (pNTS) by performing patch-clamp experiments in thin slice preparations from rat brain stem. Stimulation of single afferent fibers evoked excitatory postsynaptic currents (EPSCs) mediated by glutamate receptors of the DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid (AMPA) and N-methyl-D-aspartate types. AMPA-receptor-mediated EPSCs displayed decay time constants of 3.5 +/- 1.2 (SD) ms (13 cells), which were slow compared with EPSC decay time constants in neurons of the cerebellum or hippocampus. Slow EPSC decay was not explained by dendritic filtering, because the passive membrane properties of pNTS interneurons provided favorable voltage-clamp conditions. Also, the slowness of EPSC decay did not result from slow deactivation of AMPA receptors (0.7 +/- 0.2 ms, 5 cells), which was investigated during rapid application of agonist to outside-out patches. Comparison of AMPA receptor kinetics with EPSC decay time constants suggested that the slow time course of EPSCs resulted from the prolonged presence of glutamate in the synaptic cleft.
通过在大鼠脑干薄片标本上进行膜片钳实验，研究了孤束核小细胞部（pNTS）中间神经元的兴奋性突触传递。刺激单根传入纤维可诱发由α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）型和N-甲基-D-天冬氨酸型谷氨酸受体介导的兴奋性突触后电流（EPSCs）。AMPA受体介导的EPSCs的衰减时间常数为3.5±1.2（标准差）毫秒（13个细胞），与小脑或海马神经元中EPSC的衰减时间常数相比，该值较慢。EPSC衰减缓慢并非由树突滤波所致，因为pNTS中间神经元的被动膜特性提供了良好的电压钳制条件。此外，EPSC衰减缓慢并非源于AMPA受体的缓慢失活（0.7±0.2毫秒，5个细胞），这是在将激动剂快速施加于外向膜片时进行研究的。将AMPA受体动力学与EPSC衰减时间常数进行比较表明，EPSCs的缓慢时程是由于突触间隙中谷氨酸的持续存在时间延长所致。
