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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Modulation by D1 and D2 dopamine receptors of ATP-induced release of intracellular Ca(2+) in cultured rat striatal neurons.
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Modulation by D1 and D2 dopamine receptors of ATP-induced release of intracellular Ca(2+) in cultured rat striatal neurons.

机译:由D1和D2多巴胺受体对培养的大鼠纹状体神经元中ATP诱导的细胞内Ca(2+)释放的调节。

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The aim of the present study was to investigate, whether dopamine D1 and/or D2 receptors are able to interfere with the ATP-induced increase of the intracellular Ca(2+) concentration ([Ca(2+)](i)) in cultured striatal neurons identified by their morphological characteristics and their [Ca(2+)](i) transients in response to a high-K(+) superfusion medium. ATP appeared to release Ca(2+) mostly from an intracellular pool, since its effect was markedly depressed in the presence of cyclopiazonic acid, which is known to deplete such storage sites [Rubini, P., Pinkwart, C., Franke, H., Gerevich, Z., Norenberg, W., Illes, P., 2006. Regulation of intracellular Ca(2+) by P2Y(1) receptors may depend on the developmental stage of cultured rat striatal neurons. J. Cell. Physiol. 209, 81-93]. The mixed D1/D2 receptor agonist dopamine increased the ATP-induced [Ca(2+)](i) transients in a subpopulation of neurons. At the same time, dopamine did not alter the responses to K(+) in these cells. The selective D1 (SKF 83566) and D2 (sulpiride) receptor antagonists failed to modify the effect of ATP, but unmasked in the previously unresponsive neurons an inhibitory and facilitatory effect of dopamine, respectively. A combination of the two antagonists resulted in a failure of dopamine to modulate the [Ca(2+)](i) responses in any cell investigated. In conclusion, D1 and D2 receptors may modulate in an opposite manner the signalling pathways of P2Y(1) receptors in striatal neurons and thereby alter their development/growth or their cellular excitability and/or the release of GABA from their terminals.
机译:本研究的目的是调查多巴胺D1和/或D2受体是否能够干扰ATP诱导的细胞内Ca(2+)浓度([Ca(2 +)](i))的增加。培养的纹状体神经元,通过其形态特征和对高K(+)超融合介质的响应[Ca(2 +)](i)瞬变来识别。 ATP似乎主要从细胞内池中释放Ca(2+),因为它的作用在环吡嗪酸的存在下显着降低,已知环戊唑酸会耗尽这些存储位点[Rubini,P.,Pinkwart,C.,Franke,H ,Gerevich,Z.,Norenberg,W.,Illes,P.,2006。P2Y(1)受体对细胞内Ca(2+)的调节可能取决于培养的大鼠纹状体神经元的发育阶段。 J.细胞。生理学。 209,81-93]。混合的D1 / D2受体激动剂多巴胺增加了神经元亚群中ATP诱导的[Ca(2 +)](i)瞬变。同时,多巴胺不会改变这些细胞对K(+)的反应。选择性的D1(SKF 83566)和D2(舒必利)受体拮抗剂未能改变ATP的作用,但在先前无反应的神经元中却没有掩盖多巴胺的抑制作用和促进作用。两种拮抗剂的组合导致多巴胺无法调节所研究的任何细胞中的[Ca(2 +)](i)反应。总之,D1和D2受体可能以相反的方式调节纹状体神经元中P2Y(1)受体的信号传导途径,从而改变其发育/生长或细胞兴奋性和/或GABA从其末端释放。

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