Effects of capsaicin on Ca2+ release from the intracellular Ca2+ stores in the dorsal root ganglion cells of adult rats

被引:65
作者
Eun, SY
Jung, SJ
Park, YK
Kwak, J
Kim, SJ
Kim, J
机构
[1] Seoul Natl Univ, Coll Med, Dept Physiol, Chongno Gu, Seoul 110799, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Biophys, Chongno Gu, Seoul 110799, South Korea
[3] Dankook Univ, Coll Med, Dept Physiol, Chunan, South Korea
[4] Kangweon Natl Univ, Coll Med, Chunchon 200701, South Korea
关键词
dorsal root ganglion; capsaicin; Ca2+; Ca2+ store;
D O I
10.1006/bbrc.2001.5272
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We have investigated the effect of capsaicin on Ca2+ release from the intracellular calcium stores. Intracellular calcium concentration ([Ca2+](i)) was measured in rat dorsal root ganglion (DRG) neurons using microfluorimetry with fura-2 indicator. Brief application of capsaicin (1 muM) elevated [Ca2+](i) in Ca2+-free solution. Capsaicin-induced [Ca2+](i) transient in Ca2+-free solution was evoked in a dose-dependent manner. Resiniferatoxin, an analogue of capsaicin, also raised [Ca2+](i) in Ca2+-free solution. Capsazepine, an antagonist of capsaicin receptor, completely blocked the capsaicin-induced [Ca2+](i) transient. Caffeine completely abolished capsaicin-induced [Ca2+](i) transient. Dantrolene sodium and ruthenium red, antagonists of the ryanodine receptor, blocked the effect of capsaicin on [Ca2+](i). However, capsaicin-induced [Ca2+](i) transient was not affected by 2-APB, a membrane-permeable IP3 receptor antagonist. Furthermore, depletion of IP3-sensitive Ca2+ stores by bradykinin and phospholipase C inhibitors, neomycin, and U-73122, did not block capsaicin-induced [Ca2+](i) transient. In conclusion, capsaicin increases [Ca2+](i) through Ca2+ release from ryanodine-sensitive Ca2+ stores, but not from IP3-sensitive Ca2+ stores in addition to Ca2+ entry through capsaicin-activated nonselective cation channel in rat DRG neurons. (C) 2001 Academic Press.
引用
收藏
页码:1114 / 1120
页数:7
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