Affiliation:
1. Physiological Laboratory, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, England, UK
2. Monell Chemical Senses Center, Philadelphia, PA 19104
Abstract
In vertebrate olfactory receptor neurons (ORNs), odorant-induced activation of the transduction cascade culminates in production of cyclic AMP, which opens cyclic nucleotide–gated channels in the ciliary membrane enabling Ca2+ influx. The ensuing elevation of the intraciliary Ca2+ concentration opens Ca2+-activated Cl− channels, which mediate an excitatory Cl− efflux from the cilia. In order for the response to terminate, the Cl− channel must close, which requires that the intraciliary Ca2+ concentration return to basal levels. Hitherto, the extrusion of Ca2+ from the cilia has been thought to depend principally on a Na+–Ca2+ exchanger.In this study, we show using simultaneous suction pipette recording and Ca2+-sensitive dye fluorescence measurements that in fire salamander ORNs, withdrawal of external Na+ from the solution bathing the cilia, which incapacitates Na+–Ca2+exchange, has only a modest effect on the recovery of the electrical response and the accompanying decay of intraciliary Ca2+ concentration. In contrast, exposure of the cilia to vanadate or carboxyeosin, a manipulation designed to block Ca2+-ATPase, has a substantial effect on response recovery kinetics. Therefore, we conclude that Ca2+-ATPase contributes to Ca2+ extrusion in ORNs, and that Na+–Ca2+exchange makes only a modest contribution to Ca2+ homeostasis in this species.
Publisher
Rockefeller University Press
Cited by
19 articles.
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