Möck M, Schwarz C, Thier P
Sektion für Visuelle Sensomotorik, Neurologische Universitätsklinik Tübingen, 72076 Tubingen, Germany.
J Neurophysiol. 1997 Dec;78(6):3338-50. doi: 10.1152/jn.1997.78.6.3338.
We investigated the postsynaptic responses of neurons of the rat pontine nuclei (PN) by performing intracellular recordings in parasagittal slices of the pontine brain stem. Postsynaptic potentials (PSPs) were evoked by brief (0.1 ms) negative current pulses (10-250 microA) applied to either the cerebral peduncle or the pontine tegmentum. First, excitatory postsynaptic potentials (EPSPs) could be evoked readily from peduncular stimulation sites. These EPSPs exhibited short latencies, a nonlinear increment in response to increased stimulation currents, and an unconventional dependency on the somatic membrane potential. Pharmacological blockade of the synaptic transmission using 6,7-dinitroquinoxaline-2, 3-dione and ,-2-amino-5-phosphonovaleric acid, selective antagonists of the alpha-amino-3-hydroxy-5-methyl-4-isoxazilepropionate- (AMPA) and the N-methyl--aspartate (NMDA)-type glutamate receptors, showed that these EPSPs were mediated exclusively by excitatory amino acids via both AMPA and NMDA receptors. Moreover, the pharmacological experiments indicated the existence of voltage-sensitive but NMDA receptor-independent amplification of EPSPs. Second, stimulations at peduncular and tegmental sites also elicited inhibitory postsynaptic potentials (IPSPs) in a substantial proportion of pontine neurons. The short latencies of all IPSPs argued against the participation of inhibitory interneurons. Their sensitivity to bicuculline and reversal potentials around -70 mV suggested that they were mediated by gamma-aminobutyric acid-A (GABAA) receptors. In addition to single PSPs, sequences consisting of two to four distinct EPSPs could be recorded after stimulation of the cerebral peduncle. Most remarkably, the onset latencies of the following EPSPs were multiples of the first one indicating the involvement of intercalated synapses. Finally, we used the classic paired-pulse paradigm to study whether the temporal structure of inputs influences the synaptic transmission onto pontine neurons. Pairs of electrical stimuli applied to the cerebral peduncle resulted in a marked enhancement of the amplitude of the second EPSP for interstimulus intervals of 10-100 ms. Delays >200 ms left the EPSP amplitude unaltered. These data provide evidence for a complex synaptic integration and an intrinsic connectivity within the PN too elaborate to support the previous notion that the PN are simply a relay station.
我们通过在脑桥脑干矢状旁切片中进行细胞内记录,研究了大鼠脑桥核(PN)神经元的突触后反应。突触后电位(PSP)由施加到大脑脚或脑桥被盖的短暂(0.1毫秒)负电流脉冲(10 - 250微安)诱发。首先,从大脑脚刺激部位很容易诱发兴奋性突触后电位(EPSP)。这些EPSP表现出短潜伏期,对增加的刺激电流呈非线性增加,并且对体细胞膜电位有非常规依赖性。使用6,7 - 二硝基喹喔啉 - 2,3 - 二酮和α - 氨基 - 3 - 羟基 - 5 - 甲基 - 4 - 异恶唑丙酸酯(AMPA)及N - 甲基 - D - 天冬氨酸(NMDA)型谷氨酸受体的选择性拮抗剂 - 2 - 氨基 - 5 - 磷酸戊酸对突触传递进行药理学阻断,结果表明这些EPSP完全由兴奋性氨基酸通过AMPA和NMDA受体介导。此外,药理学实验表明存在电压敏感但与NMDA受体无关的EPSP放大。其次,在大脑脚和被盖部位的刺激也在相当一部分脑桥神经元中诱发了抑制性突触后电位(IPSP)。所有IPSP的短潜伏期排除了抑制性中间神经元参与的可能性。它们对荷包牡丹碱的敏感性以及约 - 70毫伏的反转电位表明它们由γ - 氨基丁酸 - A(GABAA)受体介导。除了单个PSP外,在刺激大脑脚后还可以记录到由两到四个不同EPSP组成的序列。最值得注意的是,后续EPSP的起始潜伏期是第一个的倍数,表明存在插入突触的参与。最后,我们使用经典的配对脉冲范式来研究输入的时间结构是否影响到脑桥神经元的突触传递。施加到大脑脚的成对电刺激在10 - 100毫秒的刺激间隔内导致第二个EPSP的幅度显著增强。延迟>200毫秒时,EPSP幅度不变。这些数据为PN内复杂的突触整合和内在连接性提供了证据,其复杂性远超之前认为PN仅仅是一个中继站的观点。