Roberts M L, Iwatsuki N, Petersen O H
Pflugers Arch. 1978 Sep 6;376(2):159-67. doi: 10.1007/BF00581579.
Segments of mouse parotid were placed in a superfusion chamber. Surface acini were impaled by one or two micro-electrodes for measurement of membrane potential and resistance. The acinus under investigation was stimulated by micro-iontophoretic application of acetylcholine (ACh) or adrenaline. Neighbouring acinar cells were electrically coupled. Electrical coupling between acinar cells only occurred within restricted domains probably corresponding to an acinus or a group of acini. Passing direct current through one intracellular electrode, the resting potential of an acinus could be set at desired levels and the dependency of the ACh-evoked potential change on the resting potential investigated. The ACh null potential (initial effect) was about--60 mV. A delayed hyperpolarizing effect of ACh could not be reversed. The initial ACh-evoked potential change was sensitive to alterations in extracellular Na, K and Cl concentration. The delayed ACh-evoked hyperpolarization was blocked by ouabain, exposure to Na-free or K-free solutions. It is concluded that ACh increases mainly K and Na membrane conductance causing K efflux and Na influx with a subsequent Na activation of an electrogenic Na pump.
将小鼠腮腺组织切片置于灌流室中。用一根或两根微电极刺入表面腺泡以测量膜电位和电阻。通过微离子电泳施加乙酰胆碱（ACh）或肾上腺素刺激所研究的腺泡。相邻腺泡细胞存在电耦联。腺泡细胞之间的电耦联仅发生在可能对应于一个腺泡或一组腺泡的受限区域内。通过一个细胞内电极通直流电，可将腺泡的静息电位设定在所需水平，并研究ACh诱发的电位变化对静息电位的依赖性。ACh零电位（初始效应）约为 -60 mV。ACh的延迟超极化效应不可逆转。ACh诱发的初始电位变化对细胞外Na、K和Cl浓度的改变敏感。延迟的ACh诱发的超极化被哇巴因、暴露于无Na或无K溶液所阻断。结论是，ACh主要增加K和Na膜电导，导致K外流和Na内流，随后Na激活生电钠泵。
