Hirst G D S, Dickens E J, Edwards F R
Department of Zoology, University of Melbourne, Victoria 3010, Australia.
J Physiol. 2002 Jun 15;541(Pt 3):917-28. doi: 10.1113/jphysiol.2002.018614.
Intracellular recordings were made from isolated bundles of the circular muscle layer of guinea-pig gastric antrum and the responses produced by stimulating intrinsic nerve fibres were examined. After abolishing the effects of stimulating inhibitory nerve terminals with apamin and L-nitroarginine (NOLA), transmural nerve stimulation often evoked a small amplitude excitatory junction potential (EJP) and invariably evoked a regenerative potential. Neurally evoked regenerative potentials had similar properties to those evoked in the same bundle by direct stimulation. EJPs and neurally evoked regenerative potentials were abolished by hyoscine suggesting that both resulted from the release of acetylcholine and activation of muscarinic receptors. Neurally evoked regenerative potentials, but not EJPs, were abolished by membrane hyperpolarization, caffeine and chloride channel blockers. In the intact antrum, excitatory vagal nerve stimulation increased the frequency of slow waves. Simultaneous intracellular recordings of pacemaker potentials from myenteric interstitial cells (ICC(MY)) and slow waves showed that the onset of each pacemaker potential normally preceded the onset of each slow wave but vagal stimulation caused the onset of each slow wave to precede each pacemaker potential. Together the observations suggest that during vagal stimulation there is a change in the origin of pacemaker activity with slow waves being initiated by intramuscular interstitial cells (ICC(IM)) rather than by ICC(MY).
采用细胞内记录法,从豚鼠胃窦环形肌层的分离肌束进行记录,并检测刺激内在神经纤维所产生的反应。在用蜂毒明肽和L-硝基精氨酸(NOLA)消除刺激抑制性神经末梢的作用后,经壁神经刺激常常诱发小幅度兴奋性接头电位(EJP),并总是诱发再生电位。神经诱发的再生电位与同一肌束直接刺激所诱发的再生电位具有相似的特性。东莨菪碱可消除EJP和神经诱发的再生电位,提示二者均由乙酰胆碱释放和毒蕈碱受体激活所致。神经诱发的再生电位可被膜超极化、咖啡因和氯通道阻滞剂消除,但EJP不受影响。在完整的胃窦中,迷走神经兴奋性刺激可增加慢波频率。同时对肌间神经丛间质细胞(ICC(MY))的起搏电位和慢波进行细胞内记录,结果显示每个起搏电位的起始通常先于每个慢波的起始,但迷走神经刺激导致每个慢波的起始先于每个起搏电位。这些观察结果共同表明,在迷走神经刺激期间,起搏活动的起源发生了变化,慢波由肌内间质细胞(ICC(IM))而非ICC(MY)起始。