Bergamaschi S, Trabucchi M, Battaini F, Parenti M, Schettini G, Meucci O, Govoni S
Institute of Pharmacological Sciences, University of Milan, Italy.
Eur Neurol. 1990;30 Suppl 2:16-20; discussion 39-41. doi: 10.1159/000117186.
The present study investigates the effect of G protein activation on dihydropyridine recognition sites in PC12 cell membranes. The addition of a stable analogue of GTP, GMP-PNP, increases the displacement of tritiated PN 200-110 produced by Bay K 8644 without modifying the one produced by nitrendipine. This effect is prevented by Pertussis toxin treatment. Functional studies based on the measurement of intracellular calcium concentrations by means of the fura 2 technique show that Pertussis toxin reduces the ability of Bay K8644 to potentiate the increase of cytosolic calcium elicited by 80 mM K+. The results support the hypothesis that a G protein may modulate the activity of voltage-dependent, dihydropyridine-sensitive calcium channels.
本研究调查了G蛋白激活对PC12细胞膜中二氢吡啶识别位点的影响。添加GTP的稳定类似物GMP-PNP，可增加由Bay K 8644引起的氚标记PN 200-110的置换，而不改变由尼群地平引起的置换。百日咳毒素处理可阻止这种效应。基于用fura 2技术测量细胞内钙浓度的功能研究表明，百日咳毒素降低了Bay K8644增强由80 mM K+引起的胞质钙增加的能力。这些结果支持了一种假设，即G蛋白可能调节电压依赖性、二氢吡啶敏感的钙通道的活性。
