Effect of lidocaine on intracellular calcium dynamics of superiol cervical garglia

腺苷-5'-三磷酸腺苷（ATP）从神经元和非神经元组织释放，与细胞表面受体相互作用，产生广泛的生理反应。本研究探讨了颈上神经节（SCG）细胞是否对ATP有反应。为此，动态。用激光扫描共聚焦显微镜分析了完整SCG神经元和卫星细胞胞内钙离子浓度（[Ca^<2+>]_i）的变化。ATP使神经元和卫星细胞中的[Ca^<2+>]_i升高；最初，ATP诱导卫星细胞增加，随后，在神经元中观察到[Ca^<2+>]_i的变化。P1嘌呤受体激动剂对这一过程没有影响，但P2嘌呤受体激动剂诱导[Ca^<2+>]_i升高，舒拉敏完全抑制atp诱导的神经元和卫星细胞[Ca^<2+>]_i动力学。在卫星细胞中，Ca^<2+>阻断剂和去除细胞外Ca，而不是thapsigarin预处理，可以消除atp诱导的[Ca^<2+>]_i动力学。相比之下，thapsigargin预处理可消除atp诱导的神经元[Ca^<2+>]_i动力学。活性蓝-2单独抑制atp诱导的神经元反应。尿苷-5′-三磷酸引起神经元[Ca^<2+>]_i升高，α，β-亚甲基ATP引起卫星细胞[Ca^<2+>]_i升高。我们得出结论，神经元主要通过P2Y嘌呤受体响应细胞外ATP，卫星细胞通过P2X嘌呤受体响应。ATP诱导神经周围细胞a [Ca^<2+>]_i升高。Ca2+通道阻滞剂和去除细胞外Ca2+，而不是thapsigarin预处理，可以消除atp诱导的[Ca2+]i动力学。这表明[Ca2+]i的增加是由于细胞外Ca2+的流入。腺苷-5'-二磷酸也引起[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没有。尿苷-5′-三磷酸对[Ca2+]i无显著影响，但α、β -亚甲基ATP引起[Ca2+]i升高。综上所述，神经周围细胞主要通过P2X受体响应细胞外ATP。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