Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E6BT, UK.
J Mol Neurosci. 2010 Jul;41(3):340-6. doi: 10.1007/s12031-010-9377-2. Epub 2010 May 6.
This article summarizes some of the effects of stimulating muscarinic receptors on nerve cell activity as observed by recording from single nerve cells and cholinergic synapses in the peripheral and central nervous sytems. It addresses the nature of the muscarinic receptor(s) involved and the ion channels and subcellular mechanisms responsible for the effects. The article concentrates on three effects: postsynaptic excitation, postsynaptic inhibition, and presynaptic (auto) inhibition. Postsynaptic excitation results primarily from the inhibition of potassium currents by M(1)/M(3)/M(5) receptors, consequent upon activation of phospholipase C by the G protein Gq. Postsynaptic inhibition results from M2-activation of inward rectifier potassium channels, consequent upon activation of Gi. Presynaptic inhibition results from M(2) or M(4) inhibition of voltage-gated calcium channels, consequent upon activation of Go. The segregation receptors, G proteins and ion channels, and the corelease of acetylcholine and glutamate from cholinergic fibres in the brain are also discussed.
本文总结了通过记录外周和中枢神经系统中的单个神经元和胆碱能突触,观察到的刺激毒蕈碱受体对神经细胞活动的一些影响。它涉及到所涉及的毒蕈碱受体(s)的性质,以及负责这些影响的离子通道和亚细胞机制。本文集中讨论了三种效应:突触后兴奋、突触后抑制和突触前(自)抑制。突触后兴奋主要是由于 M(1)/M(3)/M(5)受体抑制钾电流,这是由于 G 蛋白 Gq 激活磷脂酶 C 所致。突触后抑制是由于 M2 激活内向整流钾通道,这是由于 Gi 激活所致。突触前抑制是由于 M(2)或 M(4)抑制电压门控钙通道,这是由于 Go 激活所致。本文还讨论了分离受体、G 蛋白和离子通道,以及脑内胆碱能纤维中乙酰胆碱和谷氨酸的共释放。