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.
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