维拉帕米和地尔硫卓N -的影响,P和q型钙通道中介在大鼠纹状体多巴胺的释放。

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娜·杜波夫D, Milde,安德烈亚斯K,乌鸦U

维拉帕米和地尔硫卓N -的影响,P和q型钙通道中介在大鼠纹状体多巴胺的释放。

Br J杂志。1999年5月,127 (2):576 - 82。doi: 10.1038 / sj.bjp.0702574。

PubMed ID

10385261 (在PubMed

]

文摘

1。维拉帕米和地尔硫卓的假定的抑制性影响神经元non-L-type Ca2 +渠道调查研究了其对K + -或veratridine-evoked的影响[3 h]多巴胺([3 h] - da)在大鼠纹状体片。参与的N, P和q型渠道被确认的敏感性[3 h] - da的释放omega-conotoxin GVIA (omega-CTx-GVIA) omega-agatoxin IVA (omega-Aga-IVA)和omega-conotoxin MVIIC (omega-CTx-MVIIC),分别。2。氯化钾(50毫米)诱发[3 h] - da的释放被废除的Ca2 +的缺席,并对dihydropyridines (30 microM)。这是明显被omega-CTx-GVIA (1 microM) omega-Aga-IVA (30 nM),确认被废除omega-CTx-MVIIC (3 microM)指示的N, P和q型通道亚型。3所示。维拉帕米和地尔硫卓抑制K +诱发[3 h] - da浓度的方式发布。维拉帕米和地尔硫卓的抑制效应(每30 microM)完全添加剂的影响omega-CTx-GVIA (1 microM)而co-application omega-Aga-IVA (30 nM)仅omega-Aga-IVA产生类似的效果。4所示。 As shown previously, veratridine-evoked [3H]-DA release in Ca2+ containing medium exclusively involves Q-type Ca2+ channels. Here, diltiazem (30 microM) did not inhibit veratridine-evoked [3H]-DA release, whereas verapamil (30 microM) partially inhibited it, indicating possible involvement of Q-type channels in verapamil-induced inhibition. However, verapamil (30 microM) inhibited this release even in the absence of extracellular Ca2+, suggesting that Na+ rather than Q-type Ca2+ channels are involved. 5. Taken together, our results suggest that verapamil can block P- and at higher concentrations possibly N- and Q-type Ca2+ channels linked to [3H]-DA release, whereas diltiazem appears to block P-type Ca2+ channels only.

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药物

维拉帕米

药物靶点

药物	目标	类	生物	药理作用	行动
维拉帕米	压敏电阻器n型钙通道亚基alpha-1B	蛋白质	人类	未知的	抑制剂	细节
维拉帕米	压敏电阻器P / q型钙通道亚基alpha-1A	蛋白质	人类	未知的	抑制剂	细节