Myers A C, Undem B J
Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224, USA.
Am J Physiol. 1996 Apr;270(4 Pt 1):L630-6. doi: 10.1152/ajplung.1996.270.4.L630.
Muscarinic receptor regulation of synaptic transmission in guinea pig bronchial parasympathetic ganglia was evaluated with the use of intracellular recording of the intrinsic ganglion neurons. Methacholine (1 microM) decreased the amplitude of vagus nerve-stimulated fast excitatory postsynaptic potentials (fEPSP) by 33 and 46% (at 0.8 and 8.0 Hz, respectively) but had no effect on the amplitude of the depolarizations evoked by a bath-applied nicotinic receptor agonist. Methoctramine (1 microM) inhibited methacholine's effect on fEPSP but alone did not influence the magnitude of the fEPSP evoked by vagus nerve stimulation. Methacholine (10 microM) depolarized a subpopulation of neurons (approximately 4 mV), which was blocked by pirenzepine (0.1 microM). In other neurons, either no effect or a small (1-5 mV) hyperpolarization was noted. Cholinergic contractions of bronchial smooth muscle elicited by electrical field stimulation were potentiated by methoctramine to the same extent as those evoked by vagus nerve (preganglionic) stimulation. The data indicate that M2 receptor activation can lead to inhibition of presynaptic acetylcholine release and consequently a significant inhibition of synaptic transmission in bronchial parasympathetic ganglia. The physiological role of this neuromodulatory effect appears limited, however, when studied in the in vitro setting.
利用豚鼠支气管副交感神经节内源性神经节神经元的细胞内记录，评估了毒蕈碱受体对突触传递的调节作用。乙酰甲胆碱（1微摩尔）使迷走神经刺激诱发的快速兴奋性突触后电位（fEPSP）幅度分别降低33%和46%（分别在0.8赫兹和8.0赫兹时），但对浴用烟碱受体激动剂诱发的去极化幅度没有影响。甲溴东莨菪碱（1微摩尔）抑制了乙酰甲胆碱对fEPSP的作用，但单独使用时并不影响迷走神经刺激诱发的fEPSP幅度。乙酰甲胆碱（10微摩尔）使一部分神经元去极化（约4毫伏），这一作用被哌仑西平（0.1微摩尔）阻断。在其他神经元中，要么没有作用，要么观察到轻微（1 - 5毫伏）的超极化。电场刺激诱发的支气管平滑肌胆碱能收缩被甲溴东莨菪碱增强的程度与迷走神经（节前）刺激诱发的相同。数据表明，M2受体激活可导致突触前乙酰胆碱释放受到抑制，从而显著抑制支气管副交感神经节中的突触传递。然而，在体外实验环境中研究时，这种神经调节作用的生理作用似乎有限。
