Activity-dependent enhancement of miniature excitatory postsynaptic current amplitude and its modulation by protein kinase C in cultured rat sympathetic neurons.

A high K+ solution increased the frequency of miniature excitatory postsynaptic currents (MEPSCs) and intracellular Ca2+ concentration ([Ca2+]i) in cultured rat sympathetic neurons. Repetition or continuation of high K+ treatment increased MEPSC amplitude, acetylcholine-induced currents and the averaged rise in [Ca2+]i per single MEPSC. The enhancement of MEPSCs lasted over 30 min and was inhibited by intracellular BAPTA and phorbol ester, but not by atropine. The results suggest that repeated Ca2+ entry through the channel pore of nicotinic acetylcholine receptor enhances the efficacy of its opening and the activation of protein kinase C inhibits the enhancement.