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Activation of protein kinase C potentiates postsynaptic acetylcholine response at developing neuromuscular synapses
Author(s) -
Fu WenMei,
Lin JiannLiang
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13869.x
Subject(s) - staurosporine , protein kinase c , postsynaptic potential , long term potentiation , acetylcholine , phorbol , medicine , endocrinology , synaptogenesis , neurotransmission , neuromuscular junction , biology , chemistry , microbiology and biotechnology , neuroscience , kinase , receptor
1 Phorbol 12‐myristate 13‐acetate (TPA, 1 μ m ) and phorbol 12,13‐dibutyrate (PDBu, 2 μ m ), activators of protein kinase C (PKC), increased the mean amplitude and decay time of the spontaneous synaptic currents of Xenopus nerve‐muscle coculture, whereas, 4α‐phorbol (2 μ m ) which is an inactive phorbol analogue had no effect. 2 Staurosporine (0.5 μ m ) and H‐7 (10 μ m ), inhibitors of PKC, inhibited the potentiation effects of TPA on the spontaneous synaptic currents. 3 Effects of TPA on the postsynaptic acetylcholine (ACh) sensitivity were examined by iontophoresis of ACh to the surface of embryonic muscle cells of 1‐day‐old Xenopus cultures. TPA increased both the amplitude and decay time of ACh‐induced whole‐cell currents in isolated myocytes. 4 TPA concentration‐dependently increased the mean open time of low‐conductance ACh channels but did not affect those of high‐conductance ACh channels. PDBu but not 4α‐phorbol exhibited similar effects to TPA. Staurosporine and H‐7 inhibited the increasing effects of TPA. 5 These results suggest that activation of PKC might be involved in synaptogenesis at developing neuromuscular synapses by the postsynaptic potentiation of ACh sensitivity.