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辣椒素对成年大鼠背根神经节细胞细胞内钙库钙释放的影响。

Effects of capsaicin on Ca(2+) release from the intracellular Ca(2+) stores in the dorsal root ganglion cells of adult rats.

作者信息

Eun S Y, Jung S J, Park Y K, Kwak J, Kim S J, Kim J

机构信息

Department of Physiology, Department of Biophysics, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul, 110-799, Korea.

出版信息

Biochem Biophys Res Commun. 2001 Aug 3;285(5):1114-20. doi: 10.1006/bbrc.2001.5272.

DOI:10.1006/bbrc.2001.5272
PMID:11478769
Abstract

We have investigated the effect of capsaicin on Ca(2+) release from the intracellular calcium stores. Intracellular calcium concentration (Ca(2+)) was measured in rat dorsal root ganglion (DRG) neurons using microfluorimetry with fura-2 indicator. Brief application of capsaicin (1 microM) elevated Ca(2+) in Ca(2+)-free solution. Capsaicin-induced Ca(2+) transient in Ca(2+)-free solution was evoked in a dose-dependent manner. Resiniferatoxin, an analogue of capsaicin, also raised Ca(2+) in Ca(2+)-free solution. Capsazepine, an antagonist of capsaicin receptor, completely blocked the capsaicin-induced Ca(2+) transient. Caffeine completely abolished capsaicin-induced Ca(2+) transient. Dantrolene sodium and ruthenium red, antagonists of the ryanodine receptor, blocked the effect of capsaicin on Ca(2+). However, capsaicin-induced Ca(2+) transient was not affected by 2-APB, a membrane-permeable IP(3) receptor antagonist. Furthermore, depletion of IP(3)-sensitive Ca(2+) stores by bradykinin and phospholipase C inhibitors, neomycin, and U-73122, did not block capsaicin-induced Ca(2+) transient. In conclusion, capsaicin increases Ca(2+) through Ca(2+) release from ryanodine-sensitive Ca(2+) stores, but not from IP(3)-sensitive Ca(2+) stores in addition to Ca(2+) entry through capsaicin-activated nonselective cation channel in rat DRG neurons.

摘要

我们研究了辣椒素对细胞内钙库释放钙离子的影响。使用fura-2指示剂通过微量荧光法在大鼠背根神经节(DRG)神经元中测量细胞内钙浓度(Ca(2+))。在无钙溶液中短暂施加辣椒素(1 microM)可升高Ca(2+)。辣椒素在无钙溶液中诱导的Ca(2+)瞬变呈剂量依赖性。辣椒素类似物树脂毒素在无钙溶液中也能升高Ca(2+)。辣椒素受体拮抗剂辣椒平完全阻断了辣椒素诱导的Ca(2+)瞬变。咖啡因完全消除了辣椒素诱导的Ca(2+)瞬变。ryanodine受体拮抗剂丹曲林钠和钌红阻断了辣椒素对Ca(2+)的作用。然而,辣椒素诱导的Ca(2+)瞬变不受膜通透性IP(3)受体拮抗剂2-APB的影响。此外,缓激肽和磷脂酶C抑制剂新霉素以及U-73122对IP(3)敏感钙库的耗竭并未阻断辣椒素诱导的Ca(2+)瞬变。总之,辣椒素通过从ryanodine敏感钙库释放钙离子增加Ca(2+),但不是通过IP(3)敏感钙库,此外还通过大鼠DRG神经元中辣椒素激活的非选择性阳离子通道进入钙离子。

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