Effect of lidocaine on intracellular calcium dynamics of superiol cervical garglia

从神经元和非神经元组织释放的腺苷-5 '-三磷酸（ATP）与细胞表面受体相互作用以产生广泛的生理反应。本研究探讨了颈上级神经节（SCG）细胞是否对ATP产生反应的问题。为此，动态。用激光扫描共聚焦显微镜观察神经元和卫星细胞内钙离子浓度（[Ca^2+] i）的变化。ATP使神经元和卫星细胞内[Ca^<2+>] i增加，ATP首先引起卫星细胞内[Ca^<2+>] i增加，随后观察到神经元内[Ca^<2+>] i的变化。P1嘌呤受体激动剂对这一过程无影响，而P2嘌呤受体激动剂可引起神经元和卫星细胞内[Ca ^<2 +>]_i升高，苏拉明完全抑制ATP诱导的[Ca^<2 +>]_i动态变化。 ...更多信息 ATP诱导的[Ca^<2+>]_i动态。与此相反，thapsiglavin预处理可消除ATP诱导的神经元[Ca^<2+>]_i动态。反应蓝-2抑制ATP诱导的神经元反应。尿苷三磷酸引起神经元[Ca^<2+>]_i增加，α，β-亚甲基ATP引起卫星细胞[Ca^<2+>]_i增加，说明神经元主要通过P2 Y嘌呤受体对细胞外ATP产生反应，卫星细胞主要通过P2 X嘌呤受体对细胞外ATP产生反应，ATP引起神经束膜细胞[Ca^<2+>]_i增加。Ca 2+通道阻断剂和细胞外Ca 2+的清除可抑制ATP诱导的[Ca 2 +]i动态变化，但毒胡萝卜素预处理对[Ca 2 +]i动态变化无影响。这表明[Ca ~（2+）]i的增加是由于细胞外Ca ~（2+）的内流。腺苷-5 '-二磷酸也引起[Ca ~（2+）]i的增加，但P1受体激动剂对[Ca ~（2+）]i动态的影响很小。苏拉明完全抑制ATP诱导的[Ca ~（2+）]i动态，但活性蓝2没有。尿苷-5 '-三磷酸对[Ca ~（2+）]i无明显影响，但α，β-亚甲基ATP可引起[Ca ~（2+）]i升高。总之，神经束膜细胞主要通过P2 X受体对细胞外ATP作出反应。少

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