Abstract

Purinoceptor agonists produced potassium currents with the order of potency: ATP>adenosine=ADP=AMP> β, γ-methylene ATP, while a small response or no response was induced by 2-methylthio ATP, UTP, or α, β-methylene ATP. The response induced by β, γ-methylene ATP was completely inhibited in the presence of α, β-methylene ATP, suggesting that the relevant receptor for these agonists was a P 3 purinoceptor. ATP induced currents with a latency of 24 s and the currents were not induced in defolliculated oocytes. The currents were not affected by either the G i/o-protein inhibitor, pertussis toxin (PTX), or the selective cAMP-dependent protein kinase inhibitor, H-89, or the phospholipase C (PLC) inhibitor, neomycin, or the phospholipase A 2 (PLA 2) inhibitor, 4-bromophenacyl bromide. The currents were enhanced by the selective protein kinase C (PKC) inhibitor, GF109203X, but otherwise, they were reduced by the potent PKC activator, 12- O-tetradecanoylphorbol-13-acetate. The results of the present study suggest that a P 3 purinoceptor in the follicle cell layer of oocytes is involved in activation of potassium channels and that the evoked currents are regulated by PLC/PLA 2-independent PKC activation.

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