Soja P J, Morales F R, Baranyi A, Chase M H
Brain Research Institute, UCLA School of Medicine 90024.
Brain Res. 1987 Oct 13;423(1-2):353-8. doi: 10.1016/0006-8993(87)90862-6.
The present study was performed to generate data implicating glycine or gamma-aminobutyric acid as neurotransmitter candidates mediating the IPSPs which are recorded in lumbar motoneurons following electrical stimulation of the nucleus reticularis gigantocellularis (NRGc) during the atonia of active sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in unanesthetized, normally respiring cats during naturally occurring states of active sleep, while inhibitory amino acid antagonists were microiontophoretically released next to the recorded cell. Electrical stimuli, applied to the NRGc during active sleep under drug-free conditions, evoked inhibitory postsynaptic potentials (IPSPs) in all of the lumbar motoneurons which were examined. These NRGc-induced IPSPs exhibited an average latency-to-onset of 26.6 +/- 1.3 ms, a latency-to-peak of 42.5 +/- 1.3 ms, an average amplitude of 3.9 +/- 0.4 mV and a duration of 34.4 +/- 2.1 ms. Strychnine, when applied microiontophoretically, abolished or markedly suppressed these NRGc-induced IPSPs. In contrast, the microiontophoretic application of picrotoxin or bicuculline methiodide failed to block these IPSPs. To the extent that strychnine may be considered to be a specific antagonist of glycine, the present results suggest that glycine (or a structurally related amino acid) participates in the generation of NRGc-induced IPSPs during the atonia of active sleep.
本研究旨在生成数据,表明甘氨酸或γ-氨基丁酸作为神经递质候选物,介导在主动睡眠无张力期间电刺激巨细胞网状核(NRGc)后在腰运动神经元中记录到的抑制性突触后电位(IPSPs)。因此,在未麻醉、正常呼吸的猫处于自然发生的主动睡眠状态时,从腰运动神经元获得细胞内记录,同时在记录的细胞旁微量离子电泳释放抑制性氨基酸拮抗剂。在无药物条件下的主动睡眠期间,对NRGc施加电刺激,在所有被检查的腰运动神经元中诱发抑制性突触后电位(IPSPs)。这些由NRGc诱导的IPSPs的平均起始潜伏期为26.6±1.3毫秒,峰值潜伏期为42.5±1.3毫秒,平均幅度为3.9±0.4毫伏,持续时间为34.4±2.1毫秒。当微量离子电泳应用士的宁时,消除或显著抑制了这些由NRGc诱导的IPSPs。相比之下,微量离子电泳应用印防己毒素或甲碘化荷包牡丹碱未能阻断这些IPSPs。就士的宁可被视为甘氨酸的特异性拮抗剂而言,目前的结果表明甘氨酸(或结构相关的氨基酸)在主动睡眠无张力期间参与了由NRGc诱导的IPSPs的产生。