Pivovarov A S, Drozdova E I, Kotliar B I
Nauchnye Doki Vyss Shkoly Biol Nauki. 1989(10):54-8.
A voltage clamp technique on identified Helix lucorum's RPa3 and LPa3 neurons has been used to negate the effect of protein kinase C on extinction of response to repeated iontophoretic applications of acetylcholine to soma. Extracellular influence of phorbol ether, protein kinase C activator (12-O-tetradecanoylphorbol-13-acetate, 0.1-10 mumol/l), or polymyxin B, its blocker (100-500 mumol/l), do not affect the extinction of acetylcholine-induced neuronal response. The data show that protein kinase C is not involved into molecular mechanisms responsible for the regulation of short-term plasticity of RPa3 and LPa3 neuronal cholinoreceptors in Helix lucorum.
运用电压钳技术对已鉴定的皱襞蛞蝓的RPa3和LPa3神经元进行研究，以消除蛋白激酶C对重复离子电渗法向胞体施加乙酰胆碱所引起反应消退的影响。佛波酯（蛋白激酶C激活剂，12 - O - 十四酰佛波醇 - 13 - 乙酸酯，0.1 - 10 μmol/l）或其阻断剂多粘菌素B（100 - 500 μmol/l）的细胞外影响，并不影响乙酰胆碱诱导的神经元反应的消退。数据表明，蛋白激酶C不参与负责调节皱襞蛞蝓RPa3和LPa3神经元胆碱能受体短期可塑性的分子机制。
