Colchicine alters apamin receptors, electrical activity, and skeletal muscle relaxation
Autor: | Maria I. Behrens, Cecilia Vergara, Beatriz U. Ramirez |
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Rok vydání: | 1993 |
Předmět: |
Male
medicine.medical_specialty Potassium Channels Physiology Muscle Relaxation Electromyography Biology Apamin Axonal Transport complex mixtures Rats Sprague-Dawley Cellular and Molecular Neuroscience chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Colchicine Relaxation (psychology) medicine.diagnostic_test Muscles musculoskeletal neural and ocular physiology Skeletal muscle Biological activity musculoskeletal system Myotonia medicine.disease Sciatic Nerve Muscle Denervation Rats Receptors Neurotransmitter Electrophysiology Endocrinology Muscle relaxation medicine.anatomical_structure chemistry Neurology (clinical) |
Zdroj: | Muscle & Nerve. 16:935-940 |
ISSN: | 1097-4598 0148-639X |
DOI: | 10.1002/mus.880160908 |
Popis: | A low conductance calcium-activated K+ channel is thought to regulate the rate of firing of several excitable cells. In skeletal muscle the expression of this channel is under nerve control. Previously, we reported that axonal flow blockade of rat nerves, induced by colchicine, caused atransient increase in muscle apamin receptors, determined by 125I-apamin binding to membrane fractions. The increase in apamin receptors was correlated with repetitive discharges resembling myotonic potentials in the electromyogram, that were blockable by apamin. Here we show that the increase in muscle apamin receptors and the alteration of the electromyogram are followed closely by a slowing of the twitch relaxation, that in turn, is decreased by apamin. Furthermore, the presence of myotonic-like alterations in the electromyogram and a slowing of muscle relaxation when muscle apaminreceptors are increased suggests that these channels may participate, amongother factors, in the generation of some kinds of myotonia. © 1993 John Wiley & Sons, Inc. |
Databáze: | OpenAIRE |
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