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Calcium-induced calcium release regulates action potential generation in guinea-pig sympathetic neurones

机译:钙诱导的钙释放调节豚鼠交感神经元的动作电位生成

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摘要

Experiments were done using guinea-pig sympathetic neurones dissociated from the stellate ganglia to establish whether calcium-induced calcium release (CICR) modulated action potential (AP) generation in mammalian neurones. Using measurements of intracellular calcium ([Ca2+]i) with the Ca2+-sensitive dye fluo-3, we demonstrated that 10 mm caffeine activated ryanodine receptors and caused a rise in [Ca2+]i in both Ca2+-containing and Ca2+-deficient solutions. We also demonstrated that combined treatment with caffeine and 1 μm thapsigargin or caffeine and 20 μm ryanodine blocked subsequent caffeine-induced elevations of [Ca2+]i. Treatment with thapsigargin, ryanodine or 200 μm Cd2+ to disrupt CICR decreased the latency to AP generation during 400 ms depolarizing current ramps using the perforated patch whole cell patch clamp in current clamp mode. Treatment with 500 μm tetraethylammonium also decreased the latency to AP generation during depolarizing current ramps in control cells, but not in cells pretreated with thapsigargin to deplete internal Ca2+ stores. In summary, we propose that an outward current, carried at least in part through BK channels, is activated by CICR at membrane voltages approaching the threshold for AP initiation and that this current opposed depolarizing current ramps applied to guinea-pig sympathetic stellate neurones.
机译:使用从星状神经节分离的豚鼠交感神经元进行实验,以确定钙诱导的钙释放(CICR)是否能调节哺乳动物神经元中的动作电位(AP)生成。使用对Ca2 +敏感的染料fluo-3对细胞内钙([Ca2 +] i)的测量,我们证明了10 mm咖啡因激活了ryanodine受体,并导致含Ca2 +的溶液和缺乏Ca2 +的溶液中[Ca2 +] i的升高。我们还证明了咖啡因和1μmthapsigargin或咖啡因和20μmryanodine的联合治疗可阻止随后咖啡因引起的[Ca2 +] i升高。在电流钳模式下,使用穿孔的贴片全细胞膜片钳,用毒胡萝卜素,ryanodine或200μmCd2 +处理以破坏CICR可以减少400 ms去极化电流斜坡期间AP产生的等待时间。在对照细胞中,用500μm四乙铵处理还可减少去极化电流斜坡期间AP生成的潜伏期,但在用毒胡萝卜素预处理以耗尽内部Ca2 +储存的细胞中却没有。总之,我们提出,至少部分通过BK通道携带的外向电流在膜电压接近AP起始阈值时被CICR激活,并且该电流与应用于豚鼠交感星状神经元的去极化电流斜坡相反。

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