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首页> 外文期刊>Journal of Cellular Physiology >Regulation of intracellular Ca2+ by P2Y1 receptors may depend on the developmental stage of cultured rat striatal neurons.
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Regulation of intracellular Ca2+ by P2Y1 receptors may depend on the developmental stage of cultured rat striatal neurons.

机译:调节细胞内钙离子的P2Y1受体可能取决于文化的发展阶段大鼠纹状体神经元。

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Mixed striatal cell cultures containing neurons and glial cells were grown either in neurobasal medium (NBM) or Dulbecco's modified Eagle's medium (DMEM). Whole-cell patch-clamp recordings indicated that, if at all, only a single, low amplitude spike was evoked shortly after starting the injection of a depolarizing current pulse into NBM neurons. In contrast, DMEM neurons fired series of high amplitude action potentials, without apparent spike frequency adaptation. The possible reason for the observed action potential failure in NBM neurons was a low density of Na+ channels per unit of membrane surface area. However, both in NBM and DMEM neurons, ATP did not induce inward current responses via P2X receptor-channels, although GABAA and N-methyl-D-aspartate (NMDA) receptor-channels could be activated by muscimol and NMDA, respectively. Ca2+ imaging experiments by means of the Fura-2 method were utilized to measure intracellular Ca2+ ([Ca2+]i) in neurons and glial cells. NBM, but not DMEM neurons responded to ATP with [Ca2+]i transients; glial cells grown in either culture medium were equally sensitive to ATP. ATP caused an increase of [Ca2+]i by a mechanism only partly dependent on external Ca2+; the residual ATP effect was blocked by cyclopiazonic acid (CPA) and was therefore due to the release of Ca2+ from its intracellular pools. The receptor involved was characterized by P2 receptor antagonists (PPADS, MRS 2179, AR-C69931MX) and was found to belong to the P2Y1 subtype. CPA caused an early [Ca2+]i response due to release from intracellular storage sites, followed by a late [Ca2+]i response due to the influx of this cation from the extracellular space, probably triggered by the opening of store-operated channels (SOCs) in the plasma membrane. It is concluded that in partial analogy with the effect of CPA, ATP releases [Ca2+]i via the Gq/phospholipase C/inositoltrisphosphate (IP3) pathway, thereby opening SOCs. It is hypothesized that this effect of ATP may have an important role for the proliferation and migration of striatal neuronal progenitors.
机译:混合纹状体包含神经元细胞培养和神经胶质细胞在neurobasal增长介质(现)或杜尔贝科的鹰的修改介质(DMEM)。表明,如果有的话,只有一个单一的低振幅峰值是诱发后不久开始去极化电流脉冲的注入到非神经元。一系列高振幅动作电位,没有明显的峰值频率适应。可能观察到的原因动作电位失败在现化神经元是一个低密度的Na +渠道的单位膜面积。然而,在现化和DMEM神经元,ATP不通过P2X内诱导电流响应receptor-channels,尽管对GABAA和n -甲基- d (NMDA) receptor-channels可以通过muscimol和门冬氨酸被激活,分别。Fura-2方法被用来测量细胞内钙离子([Ca2 +] i)在神经元和神经胶质细胞。与[Ca2 +]我瞬态;要么培养基同样敏感ATP。机制只有部分依赖外部Ca2 +;剩余被ATP的影响cyclopiazonic酸(CPA),因此是由于从其细胞内池Ca2 +的释放。P2受体参与为特征受体拮抗剂(PPADS夫人2179年,AR-C69931MX)和被发现属于P2Y1亚型。从细胞内释放存储网站,后跟一个后期由于[Ca2 +]我反应从细胞外流入的阳离子空间,可能引发的开放门店渠道(soc)等离子体膜。与注册会计师的影响,ATP释放[Ca2 +]我通过《Gq》/磷脂酶C / inositoltrisphosphate(IP3)通路,从而打开出类拔萃。假设这个ATP可能有效果核扩散和重要的作用纹状体神经祖细胞的迁移。

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