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目的探讨P物质(substanceP,SP)、蛙皮素(bombesin,BOM)对豚鼠离体肠系膜下神经节(inferiormesentericganglion,IMG)非胆碱能迟慢兴奋性突触后电位(lateslow-excitatorypostsynapticpotential,ls-EPSP)的影响。方法玻璃微电极细胞内记录技术,观察细胞的膜电位变化、ls-EPSP的幅度和时程。结果刺激突触前神经在IMG细胞上引起ls-EPSP,灌流SP和BOM后分别引起的去极化与ls-EPSP具有相关性;SP受体脱敏使SP敏感细胞的ls-EPSP减弱或消失,但不影响BOM引起的去极化;BOM受体脱敏使BOM敏感细胞的ls-EPSP减弱或消失,但不影响SP引起的去极化。结论P物质、蛙皮素通过IMG细胞膜上相应受体参与了ls-EPSP的形成,受体间无交互脱敏现象。
Objective To investigate the effects of substance P (SP) and bombesin (BOM) on lateslow-excitatory postsynaptic potential (ls-1) in inferior mesenteric ganglion (IMG) EPSP). Methods Glass microelectrode intracellular recording technique was used to observe the change of cell membrane potential and the amplitude and duration of ls-EPSP. Results The depolarization caused by presynaptic nerve stimulation of ls-EPSP, perfusion SP and BOM on IMG cells was correlated with ls-EPSP. Desensitization of SP receptor caused the ls-EPSP of SP-sensitive cells to weaken or disappear , But did not affect depolarization induced by BOM; desensitization of BOM receptors attenuated or abolished ls-EPSP of BOM-sensitive cells, but did not affect the depolarization induced by SP. Conclusion Substance P and Bombesin participate in the formation of ls-EPSP through the corresponding receptors on the cell membrane of IMG, with no desensitization between receptors.