The role of extracellular sodium in the mechanism of a neuronal in vitro circadian pacemaker

Abstract

In evaluation of whether extracellular ion concentrations or fluxes are involved in the mechanism of the circadian pacemaker in Bulla retinal neurons, previous studies have ruled out obligatory requirements for extracellular calcium and chloride. In this study, it is demonstrated that extracellular sodium and magnesium are also not requirements for and do not contribute to the circadian pacemaker mechanism. Since sodium-free solutions inhibit the output rhythm of compound action potential activity, pacemaker motion during long pulse treatments was evaluated retrospectively from the phase of the circadian rhythm subsequent to the treatment. Although some pulses of sodium-free solutions were capable of affecting pacemaker phase in a manner consistent with the stopping of pacemaker motion, these effects were reversed by elevating extracellular pH, suggesting that sodium-free solutions can only affect pacemaker motion indirectly through a previously demonstrated effect of low pH on pacemaker motion.