Effect of lidocaine on intracellular calcium dynamics of superiol cervical garglia

利多卡因对上颈神经细胞内钙动态的影响

基本信息

  • 批准号:
    13671975
  • 负责人:
  • 金额:
    $ 1.6万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2003
  • 项目状态:
    已结题

项目摘要

Adenosine-5'-triphosphate (ATP) which is released from neuronal and non-neuronal tissues interacts with cell surface receptors to produce a broad range of physiological responses. The present study addressed the issue of whether the cells of the superior cervical ganglia (SCG) respond to ATP. To this end, the dynamics. of the intracellular calcium ion concentration ([Ca^<2+>]_i) of neurons and satellite cells in intact SCG was analyzed by laser scanning confocal microscopy. ATP produced an increase of [Ca^<2+>]_i in both neurons and satellite cells; initially, ATP elicited increase in satellite cells, subsequently, a [Ca^<2+>]_i change in neurons was observed. P1 purinoceptor agonists had no effect on this process, but P2 purinoceptor agonists induced [Ca^<2+>]_i increase and suramin totally inhibited ATP-induced [Ca^<2+>]_i dynamics in both neurons and satellite cells.In satellite cells, Ca^<2+> blockers and the removal of extracellular Ca, but not thapsigargin-pretreatment, abolished … More ATP-induced [Ca^<2+>]_i dynamics. In contrast, thapsigargin-pretreatment abolished ATP-induced [Ca^<2+>]_i dynamics in neurons. Reactive blue-2 inhibited the ATP-induced reaction on neurons alone. Uridine-5'-triphosphate caused a [Ca^<2+>]_i increase in neurons and α,β-methylene ATP caused a [Ca^<2+>]_i increase in satellite cells.We concluded that neurons respond to extracellular ATP mainly via P2Y purinoceptors and that satellite cells respond via P2X purinoceptors.ATP induced a [Ca^<2+>]_i increase of perineurial cells. Ca2+ channel blockers and removing of extracellular Ca2+, but not thapsigargin pretreatment, abolished ATP-induced [Ca2+]i dynamics. This indicated that the [Ca2+]i increase was due to an influx of extracellular Ca2+. Adenosine-5'-diphosphate also elicited an increase of [Ca2+]i, but P1 receptor agonists had few effects on [Ca2+]i dynamics. Suramin totally inhibited ATP-induced [Ca2+]i dynamics, but reactive blue 2 did not. Uridine-5'-triphosphate induced no significant change in [Ca2+]i, but alpha, beta-methylene ATP caused a [Ca2+]i increase. In conclusion, perineurial cells respond to extracellular ATP mainly via P2X receptors. Less
从神经元和非神经元组织释放的 5'-三磷酸腺苷 (ATP) 与细胞表面受体相互作用,产生广泛的生理反应。本研究解决了颈上神经节 (SCG) 细胞是否对 ATP 做出反应的问题。为此,动态。通过激光扫描共聚焦显微镜分析完整SCG中神经元和卫星细胞的细胞内钙离子浓度([Ca^2+]_i)。 ATP 使神经元和卫星细胞中的 [Ca^2+]_i 增加;最初,ATP 引起卫星细胞的增加,随后,观察到神经元中的 [Ca^2+]_i 变化。 P1 嘌呤受体激动剂对此过程没有影响,但 P2 嘌呤受体激动剂诱导 [Ca^<2+>]_i 增加,苏拉明完全抑制神经元和卫星细胞中 ATP 诱导的 [Ca^<2+>]_i 动态。在卫星细胞中,Ca^<2+> 阻滞剂和细胞外 Ca 的去除,但不是毒胡萝卜素预处理,废除了…… 更多 ATP 诱导的 [Ca^2+]_i 动力学。相反,毒胡萝卜素预处理消除了神经元中ATP诱导的[Ca^2+]_i动态。 Reactive blue-2 仅抑制 ATP 诱导的神经元反应。尿苷-5'-三磷酸导致神经元中 [Ca^<2+>]_i 增加,α,β-亚甲基 ATP 导致卫星细胞中 [Ca^<2+>]_i 增加。我们得出结论,神经元主要通过 P2Y 嘌呤受体对细胞外 ATP 做出反应,卫星细胞通过 P2X 嘌呤受体做出反应。ATP 诱导 [Ca^2+]_i神经周围细胞增加。 Ca2+ 通道阻滞剂和细胞外 Ca2+ 的去除(而非毒胡萝卜素预处理)可消除 ATP 诱导的 [Ca2+]i 动力学。这表明[Ca2+]i 增加是由于细胞外Ca2+ 的流入。 5'-二磷酸腺苷也会引起 [Ca2+]i 的增加,但 P1 受体激动剂对 [Ca2+]i 动力学的影响很小。苏拉明完全抑制 ATP 诱导的 [Ca2+]i 动力学,但活性蓝 2 则不然。 5'-三磷酸尿苷未诱导 [Ca2+]i 发生显着变化,但 α,β-亚甲基 ATP 导致 [Ca2+]i 增加。总之,神经束膜细胞主要通过 P2X 受体对细胞外 ATP 做出反应。较少的

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