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Electrophysiological studies of the effect of the neuropeptide proctolin on the hyperneural muscle of Periplaneta americana (L.)
Institution:1. Laboratório de Farmacologia, Instituto Butantan, Av. Vital Brazil, 1500, 05503-900, São Paulo, Brazil;2. Laboratório de Toxinologia, Instituto Osvaldo Cruz, FIOCRUZ, Av. Brasil, 4365, 21040-900, Rio de Janeiro, Brazil;3. Instituto Nacional de Ciência e Tecnologia em Toxinas (INCTTox/CNPq), Brazil;9. Departamento de Ginecologia, Universidade Federal de Sao Paulo, Sao Paulo, SP, BR;99. Departamento de Diagnostico por Imagem, Universidade Federal de Sao Paulo, Sao Paulo, SP, BR
Abstract:The myotropic neuropeptide proctolin is, in additional to its action on proctodaeum and on some other systems, highly effective on the hyperneural muscle of Periplaneta americana and evokes long-term contractions. During this proctolin response the input resistance (Rinput) increases by about 25% accompanied by only slight depolarization. These processes require extracellular Ca2+ but are still present in Na+-free solution.Junction potentials evoked by threshold stimulation of the nerve are not affected by proctolin. Synaptic processes do not seem to be important for the proctolin action on hyperneural muscle. It is more likely that the whole membrane of the muscle fibre serves as target for proctolin. Proctolin reduces the threshold for neurally evoked muscle contractions, the only available route of excitation since the muscle fibres themselves are not electrically excitable.The K+-channel blocker 4-aminopyridine may evoke contraction as well as proctolin, but this is only a transitory response. In contrast to proctolin, 4-aminopyridine is still effective after blocking the Ca2+-channels by Co2+, but the response is smaller. Therefore proctolin seems to be primarily effective via Ca2+-channels, whereas 4-aminopyridine exerts its effects via K+-channels. The decrease in membrane conductance produced by proctolin could result from a Ca2+-dependent reduction of the K+-outward current.
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