Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension.
Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension.
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哺乳动物交感神经节因结肠扩张而产生快突触电位和慢突触电位。
DOI：
10.1073/pnas.83.6.1941
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发表时间：
1986
影响因子：
11.1
通讯作者：
Kreulen,DL
中科院分区：
文献类型：
--
作者：
Peters,S;Kreulen,DL
大肠的径向扩张使豚鼠肠系膜下神经节的神经元群产生缓慢的去极化。慢电位通常与胆碱能快电位同时发生[(兴奋性突触后电位（EPSPs]），但当所有快 EPSP 不存在时，在烟碱和毒蕈碱胆碱能拮抗剂存在下仍持续存在。扩张引起的非胆碱能慢去极化的幅度随着扩张压力的增加而增加。对于在 10-20 cm 水压下持续 1 分钟的扩张，平均去极化幅度为 3.4 mV，缓慢的去极化与膜电阻的增加有关，并且长时间的结肠扩张导致神经节细胞对肽物质 P 的脱敏使扩张引起的慢电位平均减弱 49% +/- 17%。神经节：一个先前被描述为由乙酰胆碱介导，另一个在这里描述，其递质仍有待确定，但初步证据表明其部分由 P 物质介导。非胆碱能传入途径可能增强由胆碱能机械感觉传入输入到腹部椎前交感神经节介导的肠道抑制反射。
Radial distension of the large intestine produced a slow depolarization in a population of neurons in the inferior mesenteric ganglion of the guinea pig. The slow potentials often occurred simultaneously with cholinergic fast potentials [( excitatory postsynaptic potentials (EPSPs]) yet persisted in the presence of nicotinic and muscarinic cholinergic antagonists when all fast EPSPs were absent. The amplitude of the distension-induced noncholinergic slow depolarization increased with increasing distension pressure. For distensions of 1-min duration at pressures of 10-20 cm of water, the mean depolarization amplitude was 3.4 mV. The slow depolarization was associated with an increase in membrane resistance, and prolonged periods of colon distension resulted in a tachyphylaxis of the depolarization. Desensitization of ganglion cells to the peptide substance P attenuated the distension-induced slow potential by an average of 49% +/- 17%. Thus, two colonic mechanosensory afferent pathways converge on principal ganglion cells in the inferior mesenteric ganglion: one was previously described to be mediated by acetylcholine, and the other is described here, whose transmitter remains to be determined but which preliminary evidence suggests is mediated in part by substance P. The noncholinergic afferent pathway may enhance the intestinal inhibitory reflex mediated by cholinergic mechanosensory afferent input to the abdominal prevertebral sympathetic ganglia.