Temperature-dependent calcium-induced calcium release via InsP3 receptors in mouse olfactory ensheathing glial cells
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Cooling can induce Ca2+ signaling via activation of temperature-sensitive ion channels such as TRPM8, TRPA1 and ryanodine receptor channels. Here we have studied the mechanism of cooling-evoked Ca2+ signaling in mouse olfactory ensheathing cells (OECs), a specialized type of glial cells in the olfactory nerve layer of the olfactory bulb. Reducing the temperature from above 30 àto 28 àand below triggered Ca2+ transients that persisted in the absence of external Ca2+, but were suppressed after Ca2+ store depletion by cyclopiazonic acid. Cooling-evoked Ca2+ transients were present in mice deficient of TRPM8 and TRPA1, and were not inhibited by ryanodine receptor antagonists. Inhibition of InsP3 receptors with 2-APB and caffeine entirely blocked cooling-evoked Ca2+ transients. Moderate Ca2+ increases, as evoked by flash photolysis of NP-EGTA (caged Ca2+) and cyclopiazonic acid, triggered InsP3 receptor-mediated Ca2+ release at 22 ì but not at 31 î The results suggest that InsP3 receptors mediate Ca2+-induced Ca2+ release in OECs, and that this Ca2+ release is temperature-sensitive and can be suppressed at temperatures above 28 î
© 2012 Elsevier. This is the author-manuscript version of this paper. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
Central Nervous System
Peripheral Nervous System