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The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 501-512
Copyright ©2000 by the American Physiological Society
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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