Van Coppenolle F, Ahidouch A, Guilbault P, Ouadid H
Centre de Biologie Cellulaire, SN3, USTL, Villeneuve d'Ascq, France.
Mol Cell Biochem. 1997 Mar;168(1-2):155-61. doi: 10.1023/a:1006819507785.
The effects of cyclic AMP (cAMP) and cyclic GMP (cGMP) on dihydropyridine sensitive Ca2+ channels were investigated under voltage-clamp in defolliculated Pleurodeles oocytes. Intracellular injection of cAMP or extracellular application of the permeable cAMP analogue (8-Bromo cAMP, 8Br-cAMP) decreased the Ba current (IBa). This effect on IBa was blocked by the injection of protein kinase A inhibitor. Similar results were found upon internal application of the catalytic subunit of protein kinase A. In contrast, the injection of cGMP or perfusion of 8Br-cGMP increased IBa amplitude. The increase of IBa by 8Br-cGMP was blocked by the injection of the selective inhibitor of protein kinase G (KT5823). These results support the hypothesis that the basal Ba current amplitude of Pleurodeles oocytes is under the control of Protein Kinases A (PKA) and G (PKG) activity. This regulation of Ca2+ channels by the second messengers, and particularly by cAMP may reflect an important step in the maturation processus of Pleurodeles oocytes.
在去滤泡的有尾目蝾螈卵母细胞中,利用电压钳技术研究了环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)对二氢吡啶敏感的Ca2+通道的影响。细胞内注射cAMP或细胞外应用可渗透的cAMP类似物(8-溴环磷酸腺苷,8Br-cAMP)可降低钡电流(IBa)。蛋白激酶A抑制剂的注射可阻断对IBa的这种作用。在细胞内应用蛋白激酶A的催化亚基时也发现了类似结果。相反,注射cGMP或灌注8Br-cGMP可增加IBa幅度。8Br-cGMP引起的IBa增加可被蛋白激酶G的选择性抑制剂(KT5823)的注射所阻断。这些结果支持这样的假说,即有尾目蝾螈卵母细胞的基础钡电流幅度受蛋白激酶A(PKA)和蛋白激酶G(PKG)活性的控制。第二信使,尤其是cAMP对Ca2+通道的这种调节可能反映了有尾目蝾螈卵母细胞成熟过程中的一个重要步骤。