RESUMO
Blocker of presynaptic protein kinase C isoforms, GF109203X, reduced quantal content of single and rhythmic evoked end-plate potentials. The increase in quantal content of single potentials under the effect of 4- aminopyridine was neutralized by 75% under the effect of L-type Ca(2+)-channel blocker nitrendipine and completely returned to the control level after protein kinase C inhibition with chelerythrine. Neither nitrendipine, nor GF109203X affected the potentiating effect of tetraethylammonium on quantal content of end-plate potentials. Thus, we discovered basal activity of presynaptic protein kinase C under normal conditions that is aimed at the maintenance of quantal content of evoked release. It has been concluded that 4-aminipyridine, but not tetraethylammonium, triggers Ca(2+) entry into the terminal, which activates protein kinase C and enhanced the evoked acetylcholine release.
Assuntos
Cálcio/metabolismo , Neurotransmissores/metabolismo , Proteína Quinase C/metabolismo , Sinapses/efeitos dos fármacos , Transmissão Sináptica/efeitos dos fármacos , 4-Aminopiridina/farmacologia , Animais , Benzofenantridinas/farmacologia , Bloqueadores dos Canais de Cálcio/farmacologia , Canais de Cálcio Tipo L , Sinalização do Cálcio/efeitos dos fármacos , Diafragma/efeitos dos fármacos , Diafragma/fisiologia , Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos , Potenciais Pós-Sinápticos Excitadores/fisiologia , Indóis/farmacologia , Isoenzimas/antagonistas & inibidores , Isoenzimas/metabolismo , Maleimidas/farmacologia , Camundongos , Placa Motora/efeitos dos fármacos , Placa Motora/fisiologia , Nitrendipino/farmacologia , Técnicas de Cultura de Órgãos , Bloqueadores dos Canais de Potássio/farmacologia , Proteína Quinase C/antagonistas & inibidores , Inibidores de Proteínas Quinases/farmacologia , Sinapses/enzimologia , Transmissão Sináptica/fisiologia , Tetraetilamônio/farmacologiaRESUMO
Protein kinase C blocker chelerythrine prevented the increase in quantal content of single and rhythmic evoked end-plate potentials after disinhibition of L-type Ca(2+)-channels with paxillin. Phorbol ester increased quantal content of single end-plate potentials and changed rhythmic activity of mouse motor synapses. The effects of phorbol ester were to a great extent neutralized by L-type Ca(2+)-channel blocker nitrendipine and were completely abolished by K(+)-channel blocker 4-aminopyridine. Thus, we discovered different facilitations of transmission after protein kinase C activation with calcium current through L-type channels and with phorbol ester.
