RESUMO
In order to block acetylcholine receptors of muscle, the alpha toxin of the Formosan cobra (Naja naja atra) was given intravenously to rats. Electrophysiological and pharmacological changes typical of myasthenia gravis were recorded, including decremental responses to repetitive stimuli, curare sensitivity, neostigmine reversal, and posttetanic phenomena. This model supports the concept that a reduction of available acetylcholine receptors may play an important role in myasthenia gravis.
Assuntos
Modelos Animais de Doenças , Miastenia Gravis , Receptores Colinérgicos , Venenos de Serpentes , Peçonhas , Potenciais de Ação , Animais , Curare/farmacologia , Estimulação Elétrica , Potenciais Evocados , Feminino , Contração Muscular/efeitos dos fármacos , Músculos/fisiopatologia , Miastenia Gravis/tratamento farmacológico , Miastenia Gravis/metabolismo , Miastenia Gravis/fisiopatologia , Neostigmina/uso terapêutico , Bloqueadores NeuromuscularesRESUMO
The number of acetylcholine receptors was determined in the neuromuscular junctions of eight patients with typical myasthenia gravis and in five controls, by means of (125)1-labeled alpha-bungarotoxin binding. The junctional acetylcholine receptors were reduced in the myasthenic muscles as compared with the controls. This reduction in receptors may account for the defect in neuromuscular transmission in myasthenia gravis.
