• calcium channels;
  • ACh release;
  • PMA;
  • calphostin C


Using intracellular recording, we studied how protein kinase C activity affected miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) in the neuromuscular junctions of the levator auris longus muscle from adult rats. The protein kinase C activator phorbol 12-myristate 13-acetate (PMA, 10 nM) increased the quantal content by ∼150% (P < 0.05). On the other hand, the quantal content decreased by ∼40% (P < 0.05) for all the protein kinase C inhibitors tested (Calphostin-C, 10 μM; Chelerythrine, 1 μM; Staurosporine, 200 nM). These changes in acetylcholine release were maintained at plateau for 1 to 7 h. Moreover, none of the protein kinase C activators or inhibitors used could modify the spontaneous MEPP mean size (P > 0.05). We reduced the calcium influx in nerve terminals using the P/Q-type channel blocker ω-Aga-IVA(100 nM) or with 5 mM magnesium in physiological solution. In neither situation was the quantal content modified by PMA or by CaC. However, when high Ca2+ (5 mM) was added to a preparation that was previously blocked with ω-Aga-IVA, PMA and CaC had their full effect. We conclude that under physiological conditions PKC is dependent on the calcium inflow through the P/Q-type voltage-dependent calcium channels during evoked activity and works near the maximum rate at normal external calcium concentration. Synapse 57:76–84, 2005. © 2005 Wiley-Liss, Inc.