RESUMO
Acetylcholine release from the nerve terminals of the purely cholinergic Torpedo electric organ is inhibited by morphine in a dose-dependent, naloxone-reversible fashion. In addition, it is shown that this preparation contains an enkephalin-like substance which, like acetylcholine, is present in a high concentration at the nerve terminals. These findings and the chemical homogeneity of the electric organ nerve terminals render this preparation an excellent model for the study of opiate regulation of neurotransmitter release.
Assuntos
Acetilcolina/metabolismo , Órgão Elétrico/fisiologia , Encefalinas/fisiologia , Receptores Opioides/fisiologia , Torpedo/fisiologia , Animais , Órgão Elétrico/análise , Encefalinas/isolamento & purificação , Técnicas In Vitro , Modelos Neurológicos , Sinaptossomos/análiseAssuntos
Otite Externa/diagnóstico , Doença Aguda , Adulto , Alumínio/uso terapêutico , Antibacterianos/uso terapêutico , Doença Crônica , Surdez/etiologia , Dermatite de Contato/complicações , Fármacos Dermatológicos/uso terapêutico , Diagnóstico Diferencial , Feminino , Tecido de Granulação , Humanos , Higiene , Masculino , Pessoa de Meia-Idade , Micoses/complicações , Otite Externa/etiologia , Otite Externa/microbiologia , Otite Externa/terapia , Otite Média/diagnóstico , Infecções por Pseudomonas/tratamento farmacológico , Quinolinas/uso terapêutico , Infecções Estafilocócicas/tratamento farmacológicoAssuntos
Plexo Cervical , Vértebras Cervicais , Nistagmo Patológico/complicações , Doenças da Coluna Vertebral/complicações , Vertigem/complicações , Adulto , Idoso , Audiometria , Eletroculografia , Humanos , Pessoa de Meia-Idade , Nistagmo Patológico/epidemiologia , Postura , Doenças da Coluna Vertebral/cirurgia , Vertigem/epidemiologiaRESUMO
In the present communication we report that Ca2+-dependent acetylcholine release from K+-depolarized Torpedo electric organ synaptosomes is inhibited by morphine, and that this effect is blocked by the opiate antagonist naloxone. This finding suggests that the purely cholinergic Torpedo electric organ neurons contain presynaptic opiate receptors whose activation inhibits acetylcholine release. The mechanisms underlying this opiate inhibition were investigated by comparing the effects of morphine on acetylcholine release induced by K+ depolarization and by the Ca2+ ionophore A23187 and by examining the effect of morphine on 45Ca2+ influx into Torpedo nerve terminals. These experiments revealed that morphine inhibits 45Ca2+ influx into K+-depolarized Torpedo synaptosomes and that this effect is blocked by naloxone. The effects of morphine on K+ depolarization-mediated 45Ca2+ influx and on acetylcholine release have similar dose dependencies (half-maximal inhibition at 0.5-1 microM), suggesting that opiate inhibition of release is due to blockage of the presynaptic voltage-dependent Ca2+ channel. This conclusion is supported by the finding that morphine does not inhibit acetylcholine release when the Ca2+ channel is bypassed by introducing Ca2+ into the Torpedo nerve terminals via the Ca2+ ionophore.