期刊
CELL CALCIUM
卷 52, 期 2, 页码 113-123出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2012.04.017
关键词
Olfactory ensheathing cells; Glial calcium signaling; Cold-induced calcium signaling; Inositol-1,4,5-trisphosphate receptor; Transient receptor potential channel
类别
资金
- Deutsche Forschungsgemeinschaft [GRK 845, LO 779/3]
- National Health and Medical Research Council of Australia [511006]
- Australian Research Council [DP0986294]
- Australian Research Council [DP0986294] Funding Source: Australian Research Council
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 degrees C to 28 degrees C and 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 InsP(3) 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 InsP(3) receptor-mediated Ca2+ release at 22 degrees C, but not at 31 degrees C. The results suggest that InsP(3) receptors mediate Ca2+-induced Ca2+ release in OECs, and that this Ca2+ release is temperature-sensitive and can be suppressed at temperatures above 28 degrees C. (C) 2012 Elsevier Ltd. All rights reserved.
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