Cole A E, Shinnick-Gallagher P
Nature. 1984;307(5948):270-1. doi: 10.1038/307270a0.
Slow muscarinic inhibition may be a powerful influence on membrane properties in the peripheral and central nervous system. But the location of the muscarinic receptors in sympathetic ganglia, either on interneurones or on the postganglionic membrane, and the underlying mechanism of the inhibitory response, remains controversial. In mammalian sympathetic ganglia synaptic activation of muscarinic receptors located on inhibitory interneurones was thought to release catecholamines leading to a membrane hyperpolarization called the slow inhibitory postsynaptic potential, or s.-i.p.s.p.. However, the s.-i.p.s.p. in parasympathetic ganglia and in amphibian sympathetic ganglia is due to direct monosynaptic activation of muscarinic receptors, accompanied by an increased potassium conductance (but see ref. 11), and is not mediated by catecholamines. The situation is less clear in mammalian sympathetic ganglia and monosynaptic s.-i.p.s.ps observed in other ganglia could be exceptions to the hypothesis. We showed earlier that the s.-i.p.s.p. in rabbit superior cervical ganglia is not affected by catecholamine antagonists. We now show that the s.-i.p.s.p. in a mammalian sympathetic ganglion is due to the monosynaptic activation of muscarinic receptors, probably by an increase in potassium conductance.
缓慢的毒蕈碱抑制作用可能对周围和中枢神经系统的膜特性产生强大影响。但是，毒蕈碱受体在交感神经节中的位置，无论是在中间神经元上还是在节后膜上，以及抑制反应的潜在机制，仍然存在争议。在哺乳动物交感神经节中，位于抑制性中间神经元上的毒蕈碱受体的突触激活被认为会释放儿茶酚胺，导致膜超极化，称为缓慢抑制性突触后电位，即s.-i.p.s.p.。然而，副交感神经节和两栖类交感神经节中的s.-i.p.s.p.是由于毒蕈碱受体的直接单突触激活，伴有钾电导增加（但见参考文献11），且不是由儿茶酚胺介导的。在哺乳动物交感神经节中的情况不太清楚，在其他神经节中观察到的单突触s.-i.p.s.ps可能是该假设的例外情况。我们之前表明，兔颈上神经节中的s.-i.p.s.p.不受儿茶酚胺拮抗剂的影响。我们现在表明，哺乳动物交感神经节中的s.-i.p.s.p.是由于毒蕈碱受体的单突触激活，可能是通过钾电导增加所致。
