Parotid acinar cells: ionic dependence of acetylcholine-evoked membrane potential changes

Abstract

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.

Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

“…ROBERTS et al (1978) have shown that methylsulphate substitution for Clr resulted in a shift of EAch from -63 to -77 mV. Therefore, in the absence of Cl-, A23187-evoked major current carriers must be K+ ions through the large K+ channels, which have been found in the parotid acinar cells (MARUYAMA et al, 1983a).…”

“…Therefore, when two channels are activated by the agonist, the reversal potential for the agonist-evoked current response must be at potentials between two equilibrium potentials (Eg and E01), as shown in Fig. 1 B. The reversal potential of -63 mY for the ACh-evoked voltage response in mouse parotid gland acinar cells (RoBERTS et al, 1978) could be explained by postulating the agonist-evoked inward and outward currents.…”

“…Conventional microelectrode studies of mouse parotid gland acinar cells have shown that the autonomic nerve stimulation, as well as the application of acetylcholine (ACh) or adrenaline, increases the membrane con-ductance primarily to K+ but also to other ions (RoBERTS et al, 1978;GALLACHER and PETERSEN, 1980). The recent patch-clamp single channel current recordings have shown that Cat-and voltage-activated K+ channels, with a large unit conductance, dominate in the basolateral membrane in these glands (MARUYAMA et al, 1983a).…”

Communications

“…The effect of ACh seems therefore most likely to be due to an effect on the basolateral membrane. The fact that ACh did not change the mean value of the membrane potential is not surprising since in the parotid EACh is at the value of Em (Roberts et al 1978).…”

“…In the parotid gland secretion is associated with a particularly dramatic enhancement of luminal membrane area due to the insertion of granule membrane (Amsterdam, Ohad & Schramm, 1969); electrophysiological experiments were therefore 81P PROCEEDINGS OF THE carried out on superfused segments of mouse parotid as previously described (Roberts, Iwatsuki & Petersen, 1978).…”