Effects of xenon (Xe) on whole-cell currents induced by glutamate (Glu), its three ionotropic subtypes, and GABA, as well as on the fast synaptic glutamatergic and GABAergic transmissions, were studied in the mechanically dissociated "synapse bouton preparation" of rat spinal sacral dorsal commissural nucleus (SDCN) neurons. This technique evaluates pure single or multi-synapse responses from native functional nerve endings and enables us to quantify how Xe influences pre- and postsynaptic transmissions accurately. Effects of Xe on glutamate (Glu)-, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-, kainate (KA)- and N-methyl-d-aspartate (NMDA)- and GABAA receptor-mediated whole-cell currents were investigated by the conventional whole-cell patch configuration. Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were measured as spontaneous (s) and evoked (e) EPSCs and IPSCs. Evoked synaptic currents were elicited by paired-pulse focal electric stimulation. Xe decreased Glu, AMPA, KA, and NMDA receptor-mediated whole-cell currents but did not change GABAA receptor-mediated whole-cell currents. Xe decreased the frequency and amplitude but did not affect the 1/e decay time of the glutamatergic sEPSCs. Xe decreased the frequency without affecting the amplitude and 1/e decay time of GABAergic sIPSCs. Xe decreased the amplitude and increased the failure rate (Rf) and paired-pulse ratio (PPR) without altering the 1/e decay time of both eEPSC and eIPSC, suggesting that Xe acts on the presynaptic side of the synapse. The presynaptic inhibition was greater in eEPSCs than in eIPSCs. We conclude that Xe decreases glutamatergic and GABAergic spontaneous and evoked transmissions at the presynaptic level. The glutamatergic presynaptic responses are the main target of anesthesia-induced neuronal responses. In contrast, GABAergic responses minimally contribute to Xe anesthesia.

中文翻译：

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氙在大鼠脊髓神经元的真正突触水平上调节 GABA 和谷氨酸反应。

氙 (Xe) 对由谷氨酸 (Glu)、其三种离子型亚型和 GABA 诱导的全细胞电流的影响，以及对快速突触谷氨酸能和 GABA 能传递的影响，在机械分离的“突触 bouton 制剂”中进行了研究。大鼠脊髓骶骨背连合核 (SDCN) 神经元。该技术评估来自天然功能性神经末梢的纯单突触或多突触反应，使我们能够准确量化 Xe 如何影响突触前和突触后传输。Xe 对谷氨酸 (Glu)-、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸 (AMPA)-、红藻氨酸 (KA)- 和 N-甲基-d-天冬氨酸 (NMDA)- 和 GABAA 的影响通过传统的全细胞贴片配置研究了受体介导的全细胞电流。兴奋性和抑制性突触后电流 (EPSCs 和 IPSCs) 被测量为自发 (s) 和诱发 (e) EPSCs 和 IPSCs。诱发突触电流是由成对脉冲焦点电刺激引起的。Xe 降低了 Glu、AMPA、KA 和 NMDA 受体介导的全细胞电流，但不会改变 GABAA 受体介导的全细胞电流。Xe 降低了频率和振幅，但不影响谷氨酸能 sEPSCs 的 1/e 衰减时间。Xe 在不影响 GABAergic sIPSC 的振幅和 1/e 衰减时间的情况下降低频率。Xe 在不改变 eEPSC 和 eIPSC 的 1/e 衰减时间的情况下降低了振幅并增加了故障率 (Rf) 和成对脉冲比 (PPR)，表明 Xe 作用于突触的突触前侧。eEPSCs 中的突触前抑制比 eIPSCs 更大。我们得出结论，Xe 降低了突触前水平的谷氨酸能和 GABA 能自发和诱发传输。谷氨酸能突触前反应是麻醉诱导的神经元反应的主要目标。相比之下，GABA 能反应对 Xe 麻醉的贡献很小。