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首页> 外文会议>International Conference on Basic and Systemic Mechanisms of Anesthesia >Anesthetics modulate the release of glutamate and GABA via neuronal nicotinic acetylcholine receptors
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Anesthetics modulate the release of glutamate and GABA via neuronal nicotinic acetylcholine receptors

机译：麻醉剂通过神经元烟碱乙酰胆碱受体调节谷氨酸和GABA的释放

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Inhalational general anesthetics are known to modulate the activity of various neuroreceptors and ion channels. Potentiation of the GABA_A receptor function and inhibition of the glutamate receptors received much attention. Recently, it is becoming abundantly clear that neuronal nicotinic acetylcholine receptors (nAChRs) are also an important target site of general anesthetics. Modulation of the presynaptic and preterminal nAChRs affects the release of various transmitters leading to amplification of the effects via a cascade of multisynaptic events. We studied the effects of isoflurane and sevoflurane on spontaneous miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mlPSCs) in rat cortical neurons in primary culture. The currents were recorded from bipolar and multipolar neurons using the patch clamp technique. Both isoflurane and sevolfurane at 1 MAC had essentially the same effects, hi bipolar neurons, the amplitude of mEPSCs was suppressed by anesthetics, while that of mlPSCs was augmented. These effects of anesthetics reflect direct inhibition and potentiation of the glutamate and GABAA receptors, respectively. The frequency of mEPSCs and mlPSCs of bipolar neurons was increased by 30 muM ACh, reflecting the increased release of glutamate and GABA, respectively, as a result of the activation of nAChRs. Anesthetics had no effect on the frequency when applied along. However, when anesthetics and ACh were co-applied, the frequency was increased less than that caused by ACh alone, presumably because anesthetics inhibited the activity of nAChRs. Multipolar neurons were devoid of nAChs and responded to ACh and anesthetics in the same way as that of bipolar neurons with the exception of the responses via nAChRs. hi conclusion, isoflurane and sevoflurane modulate the activity of the glutamate and GABA receptors both directly and indirectly via inhibition of nAChRs.
机译：已知吸入的一般麻醉剂调节各种神经感受器和离子通道的活性。 GABA_A受体功能的增强性和抑制谷氨酸受体的抑制得到了很多关注。最近，它变得丰富地清楚的是，神经元烟碱乙酰胆碱受体（NACHRS）也是全麻的重要靶位部位。突触前和预体NACHR的调节影响各种发射器的释放，导致通过级联的多界事件扩增效果。我们研究了异氟醚和七氟醚对原发性培养中大鼠皮质神经元的自发微型兴奋性突触激流（MEPSCs）和微型抑制突触突出电流（MLPSC）的影响。使用贴片钳技术从双极和多极神经元记录电流。在1mAM的异氟醚和Sevolph均具有基本上相同的效果，Hi Bipolar神经元，MEPSCs的幅度被麻醉剂抑制，而MLPSCS的增加是增强的。麻醉剂的这些效果分别反映了谷氨酸和GABAA受体的直接抑制和增强。双极性神经元的MEPSC和MLPSC的频率增加了30毫米ACH，分别反映了由于NACHRS的活化而增加的谷氨酸和GABA的释放。麻醉剂在施用时对频率没有影响。然而，当共同应用麻醉剂和ACH时，频率少于ACH单独引起的频率，可能因为麻醉剂抑制NACHRS的活性。多解神经元没有NACH，以与双极神经元相同的方式应对ACH和麻醉剂，除了通过NACHRS的反应。嗨结论，异氟醚和七氟醚通过抑制NACHRS直接和间接地调节谷氨酸和GABA受体的活性。

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