The intravenous anaesthetic ketamine, has been demonstrated to inhibit nicotinic acetylcholine receptor (nAChR)-mediated currents in dissociated rat intracardiac ganglion (ICG) neurons (Weber et al., 2005). This effect would be predicted to depress synaptic transmission in the ICG and would account for the inhibitory action of ketamine on vagal transmission to the heart (Inoue and König, 1988). This investigation was designed to examine the activity of ketamine on (i) postsynaptic responses to vagal nerve stimulation, (ii) the membrane potential, and (iii) membrane current responses evoked by exogenous application of ACh and nicotine in ICG neurons in situ. Intracellular recordings were made using sharp intracellular microelectrodes in a whole mount ICG preparation. Preganglionic nerve stimulation and recordings in current- and voltage-clamp modes were used to assess the action of ketamine on ganglionic transmission and nAChR-mediated responses. Ketamine attenuated the postsynaptic responses evoked by nerve stimulation. This reduction was significant at clinically relevant concentrations at high frequencies. The excitatory membrane potential and current responses to focal application of ACh and nicotine were inhibited in a concentration-dependent manner by ketamine. In contrast, ketamine had no effect on either the directly-evoked action potential or excitatory responses evoked by focal application of γ-aminobutyric acid (GABA). Taken together, ketamine inhibits synaptic transmission and nicotine- and ACh-evoked currents in adult rat ICG. Ketamine inhibition of synaptic transmission and nAChR-mediated responses in the ICG contributes significantly to its attenuation of the bradycardia observed in response to vagal stimulation in the mammalian heart.

中文翻译：

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氯胺酮抑制大鼠心内神经节原位的突触传递和烟碱乙酰胆碱受体介导的反应。

静脉麻醉剂氯胺酮已被证明能抑制离体大鼠心内神经节（ICG）神经元的烟碱乙酰胆碱受体（nAChR）介导的电流（Weber等，2005）。可以预计这种作用会抑制ICG中的突触传递，并解释氯胺酮对迷走神经向心脏传递的抑制作用（Inoue和König，1988年）。这项研究旨在检查氯胺酮对（i）迷走神经刺激的突触后反应，（ii）膜电位和（iii）外源性在ICG神经元中外源施加ACh和尼古丁引起的膜电流反应的活性。在完整的ICG制备中，使用锋利的细胞内微电极进行细胞内记录。神经节前神经刺激和电流钳和电压钳模式的记录用于评估氯胺酮对神经节传递和nAChR介导的反应的作用。氯胺酮减弱了神经刺激引起的突触后反应。在高频下，在临床相关浓度下，这种降低是显着的。氯胺酮以浓度依赖的方式抑制对乙酰胆碱和烟碱局部应用的兴奋性膜电位和电流响应。相比之下，氯胺酮对直接诱发的动作电位或因局部施用γ-氨基丁酸（GABA）引起的兴奋性反应均无影响。氯胺酮合在一起可以抑制成年大鼠ICG中的突触传递以及尼古丁和ACh诱发的电流。