Assuntos
Comunicação , Relações Dentista-Paciente , Comportamento Alimentar , Fenômenos Fisiológicos da Nutrição , Adolescente , Cariogênicos/administração & dosagem , Criança , Sacarose Alimentar/administração & dosagem , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Educação de Pacientes como AssuntoAssuntos
Auxiliares de Odontologia , Odontólogos , Doenças Profissionais/etiologia , Transtornos Traumáticos Cumulativos/etiologia , Transtornos Traumáticos Cumulativos/prevenção & controle , Ergonomia , Humanos , Doenças Musculoesqueléticas/etiologia , Doenças Musculoesqueléticas/prevenção & controle , Doenças Profissionais/prevenção & controle , Fatores de Risco , Estados Unidos , United States Occupational Safety and Health AdministrationAssuntos
Aletrinas/farmacologia , Axônios/efeitos dos fármacos , Inseticidas/farmacologia , Canais Iônicos/efeitos dos fármacos , Piretrinas/farmacologia , Sódio/metabolismo , Potenciais de Ação/efeitos dos fármacos , Animais , Axônios/fisiologia , Decapodiformes , Ácido Desoxicólico/farmacologia , Relação Dose-Resposta a Droga , Cinética , Estereoisomerismo , Tetrodotoxina/farmacologiaRESUMO
The effects of the pyrethroid insecticide tetramethrin on voltage-dependent sodium channels were studied with internally perfused crayfish giant axons. At low concentrations in the order of 10-8-10-9M, tetramethrin caused an increase in depolarizing after-potential which in turn triggered repetitive after-discharges. Under Voltage clamp conditions, the sodium current was markedly prolonged during a step depolarization, and a large and prolonged sodium tail current appeared upon step repolarization. A population of sodium channels having activation and inactivation kinetics identical to those in control axons was observed in the tetramethrin-poisoned axons, indicating that only a fraction of the channels was modified. The modified channels exhibited remarkably slow kinetics, activating with a time course of 100 msec to 2 sec and inactivating with a time course of 1-5 sec depending on the membrane potential. The voltage dependence of the modified channels was shifted in the direction of hyperpolarization by about 10-20 mV with respect to normal sodium channels. The large inward sodium tail current associated with step repolarization of the membrane decayed with a time course of 20-600 msec. A kinetic hypothesis describing the behavior of sodium channels in a tetramethrin-poisoned axon is presented and discussed in relation of the behavior of the sodium channels modified by other toxins.