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首页> 外文期刊>The European Journal of Neuroscience >Disparate cholinergic currents in rat principal trigeminal sensory nucleus neurons mediated by M1 and M2 receptors: a possible mechanism for selective gating of afferent sensory neurotransmission.
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Disparate cholinergic currents in rat principal trigeminal sensory nucleus neurons mediated by M1 and M2 receptors: a possible mechanism for selective gating of afferent sensory neurotransmission.

机译：M1和M2受体介导的大鼠主要三叉神经感觉核神经元中的胆碱能电流不同：传入感觉神经传递的选择性门控的可能机制。

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摘要

Neurons situated in the principal sensory trigeminal nucleus (PSTN) convey orofacial sensory inputs to thalamic relay regions and higher brain centres, and the excitability of these ascending tract cells is modulated across sleep/wakefulness states and during pain conditions. Moreover, acetylcholine release changes profoundly across sleep/wakefulness states and ascending sensory neurotransmission is altered by cholinergic agonists. An intriguing possibility is, therefore, that cholinergic mechanisms mediate such state-dependent modulation of PSTN tract neurons. We tested the hypotheses that cholinergic agonists can modulate PSTN cell excitability and that such effects are mediated by muscarinic receptor subtypes, using patch-clamp methods in rat and mouse. In all examined cells, carbachol elicited an electrophysiological response that was independent of action potential generation as it persisted in the presence of tetrodotoxin. Responses were of three types: depolarization, hyperpolarization or a biphasic response consisting of hyperpolarization followed by depolarization. In voltage-clamp mode, carbachol evoked corresponding inward, outward or biphasic currents. Moreover, immunostaining for the vesicle-associated choline transporter showed cholinergic innervation of the PSTN. Using muscarinic receptor antagonists, we found that carbachol-elicited PSTN neuron hyperpolarization was mediated by M2 receptors and depolarization, in large part, by M1 receptors. These data suggest that acetylcholine acting on M1 and M2 receptors may contribute to selective excitability enhancement or depression in individual, rostrally projecting sensory neurons. Such selective gating effects via cholinergic input may play a functional role in modulation of ascending sensory transmission, including across behavioral states typified by distinct cholinergic tone, e.g. sleep/wakefulness arousal levels or neuropathic pain conditions.
机译：位于主要感觉三叉神经核（PSTN）的神经元将口面感觉输入传递到丘脑中继区域和较高的大脑中枢，并且这些上升道细胞的兴奋性在整个睡眠/清醒状态下以及在疼痛状态下均受到调节。此外，乙酰胆碱的释放在整个睡眠/清醒状态中发生深刻变化，并且胆碱能激动剂改变了感觉神经的传递。因此，一种有趣的可能性是胆碱能机制介导了PSTN束神经元的这种状态依赖性调节。我们用大鼠和小鼠的膜片钳方法测试了胆碱能激动剂可以调节PSTN细胞兴奋性以及这种影响是由毒蕈碱受体亚型介导的假设。在所有检查过的细胞中，卡巴胆碱在存在河豚毒素的情况下持续引起电生理反应，而该反应与动作电位的产生无关。响应分为三种类型：去极化，超极化或由超极化然后去极化组成的双相响应。在电压钳模式下，卡巴胆碱引起相应的内，外或双相电流。此外，与囊泡相关的胆碱转运蛋白的免疫染色显示了PSTN的胆碱能神经支配。使用毒蕈碱受体拮抗剂，我们发现卡巴胆碱引起的PSTN神经元超极化是由M2受体介导的，而去极化在很大程度上是由M1受体介导的。这些数据表明，作用于M1和M2受体的乙酰胆碱可能有助于选择性地增强个体或向后投射的感觉神经元的兴奋性。经由胆碱能输入的这种选择性门控作用可以在调节上升的感觉传递中发挥功能性作用，包括跨越以独特的胆碱能音调为代表的行为状态，例如，不同的胆碱能。睡眠/清醒觉醒水平或神经性疼痛状况。

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