Amplification of odor-induced Ca2+ transients by store-operated Ca2+ release and its role in olfactory signal transduction

A critical role of Ca2+ in vertebrate olfactory receptor neurons (ORNs) is to couple odor-induced excitation to intracellular feedback pathways that a re 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 s alamander 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 comp artmentalized Ca2+ release and capacitative-like Ca2+ entry in the dendrite and soma but not in the cilia, the site of odor transduction. We deplete t he stores to show that odor stimulation causes store-dependent Ca2+ mobiliz ation. This odor-induced Ca2+ release does not seem to be necessary for gen eration of an immediate electrophysiological response, nor does it contribu te significantly to the Ca2+ transients in the olfactory cilia. Rather, it is important for amplifying the magnitude and duration of Ca2+ transients i n the dendrite and soma and is thus necessary for the spread of an odor-ind uced Ca2+ wave from the cilia to the soma. We show that this amplification process depends on Ca2+-induced Ca2+ release. The results indicate that sti mulation of ORNs with odorants can produce Ca2+ mobilization from intracell ular stores without an immediate effect on the receptor potential. Odor-ind uced, store-dependent Ca2+ mobilization may be part of a feedback pathway b y which information is transferred from the distal dendrite of an ORN to it s soma.