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J Neurophysiol 83: 501-512, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 501-512
Copyright ©2000 by the American Physiological Society

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 and 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

Zufall, Frank, Trese Leinders-Zufall, and Charles A. Greer. Amplification of Odor-Induced Ca2+ Transients by Store-Operated Ca2+ Release and Its Role in Olfactory Signal Transduction. J. Neurophysiol. 83: 501-512, 2000. 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.




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