Amplification of Odor-Induced Ca2+ Transients by Store-Operated Ca2+ Release and its Role in Olfactory Signal Transduction. Frank Zufall,1 Trese Leinders-Zufall,1 nd Charles A. Greer2,3. 1Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland, Baltimore, Maryland 21201, and 2Section of Neurobiology and 3Department of Neurosurgery, Yale University, New Haven, Connecticut 06520.
APStracts 6:0466N, 1999.
A critical role of Ca2+ in vertebrate olfactory receptor neurons (ORNs) is to couple odor-induced excitation to intracellular feedback pathways that are responsible for the regulation of the sensitivity of the sense of smell, but the role of intracellular Ca2+ stores in this process remains unclear. Using confocal Ca2+ imaging and perforated patch recording, we show that salamander ORNs contain a releasable pool of Ca2+ that can be discharged at rest by the SERCA inhibitor thapsigargin and the ryanodine receptor agonist caffeine. The Ca2+ stores are spatially restricted; emptying produces compartmentalized Ca2+ release and capacitative-like Ca2+ entry in the dendrite and soma but not in the cilia, the site of odor transduction. We deplete the stores to show that odor stimulation causes store-dependent Ca2+ mobilization. This odor-induced Ca2+ release does not seem to be necessary for generation of an immediate electrophysiological response nor does it contribute significantly to the Ca2+ transients in the olfactory cilia. Rather, it is important for amplifying the magnitude and duration of Ca2+ transients in the dendrite and soma and is thus necessary for the spread of an odor-induced Ca2+ wave from the cilia to the soma. We show that this amplification process depends on Ca2+-induced Ca2+ release. The results indicate that stimulation of ORNs with odorants can produce Ca2+ mobilization from intracellular stores without an immediate effect on the receptor potential. Odor-induced, store-dependent Ca2+ mobilization may be part of a feedback pathway by which information is transferred from the distal dendrite of an ORN to its soma.
Received 7 July 1999; accepted in final form 23 September 1999.
APS Manuscript Number J550-9.
Article publication pending Journal of Neurophysiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 21 December 1999