Dascal N, Lotan I, Gillo B, Lester H A, Lass Y
Proc Natl Acad Sci U S A. 1985 Sep;82(17):6001-5. doi: 10.1073/pnas.82.17.6001.
In Xenopus laevis oocytes, adenosine and other purinergic agonists induce a K+-conductance increase that is fully mimicked by intracellular application of cAMP. Acetylcholine suppresses the K+-conductance increase caused by adenosine, by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, or by intracellular injection of cAMP. This effect of acetylcholine is not mimicked by intracellular injection of Ca2+ or of the Ca-mobilizing agent inositol 1,4,5-trisphosphate. However, adenosine and cAMP responses are inhibited by 4 beta-phorbol 12,13-dibutyrate and 4 beta-phorbol 12-myristate 13-acetate. These results suggest that, in Xenopus oocytes, the muscarinic inhibition of purinergic and cAMP responses is mediated through the activation of the phospholipid-dependent, Ca-activated protein kinase (protein kinase C).
在非洲爪蟾卵母细胞中,腺苷及其他嘌呤能激动剂可诱导钾离子电导增加,而细胞内施加环磷酸腺苷(cAMP)可完全模拟这种增加。乙酰胆碱可抑制由腺苷、磷酸二酯酶抑制剂3 -异丁基- 1 -甲基黄嘌呤或细胞内注射cAMP所引起的钾离子电导增加。乙酰胆碱的这种作用不能通过细胞内注射钙离子或钙动员剂肌醇1,4,5 -三磷酸来模拟。然而,腺苷和cAMP反应可被4β -佛波醇12,13 -二丁酸酯和4β -佛波醇12 -肉豆蔻酸酯13 -乙酸酯抑制。这些结果表明,在非洲爪蟾卵母细胞中,毒蕈碱对嘌呤能和cAMP反应的抑制是通过磷脂依赖性、钙激活蛋白激酶(蛋白激酶C)的激活介导的。