calcimycin and Neuromuscular-Diseases

calcimycin has been researched along with Neuromuscular-Diseases* in 1 studies

Other Studies

1 other study(ies) available for calcimycin and Neuromuscular-Diseases

Article	Year
Neurogenic origin of an experimental myopathy induced by the ionophore A23187. Journal of the neurological sciences, 1985, Volume: 69, Issue:3 An experimental myopathy was induced in frog skeletal muscle incubated in vitro with the calcium ionophore A23187. This myopathy could be prevented if Ca2+ ions in the incubating medium were replaced by either Mg2+ or Co2+ ions. Similarly, preincubation of the preparation with acetylcholine (ACh) receptor blockers such as d-tubocurarine (d-TC) or alpha-bungarotoxin (alpha-BuTX) prevented the development of muscle damage. In muscles that had been previously denervated or treated with botulinum toxin (BTX) the ionophore failed to induce morphological alterations. These results suggest that spontaneous transmitter release, greatly increased by the ionophore A23187, triggers Ca2+ influx into the muscle fibres at the endplate region. Elevated levels of intracellular Ca2+ presumably activate proteolytic systems leading to myofilament disassembly. Topics: Animals; Calcimycin; Calcium; In Vitro Techniques; Microscopy, Electron; Muscles; Neuromuscular Diseases; Neuromuscular Junction; Peptide Hydrolases; Rana pipiens	1985

Article

Year

Neurogenic origin of an experimental myopathy induced by the ionophore A23187.

Journal of the neurological sciences, 1985, Volume: 69, Issue:3

An experimental myopathy was induced in frog skeletal muscle incubated in vitro with the calcium ionophore A23187. This myopathy could be prevented if Ca2+ ions in the incubating medium were replaced by either Mg2+ or Co2+ ions. Similarly, preincubation of the preparation with acetylcholine (ACh) receptor blockers such as d-tubocurarine (d-TC) or alpha-bungarotoxin (alpha-BuTX) prevented the development of muscle damage. In muscles that had been previously denervated or treated with botulinum toxin (BTX) the ionophore failed to induce morphological alterations. These results suggest that spontaneous transmitter release, greatly increased by the ionophore A23187, triggers Ca2+ influx into the muscle fibres at the endplate region. Elevated levels of intracellular Ca2+ presumably activate proteolytic systems leading to myofilament disassembly.

Topics: Animals; Calcimycin; Calcium; In Vitro Techniques; Microscopy, Electron; Muscles; Neuromuscular Diseases; Neuromuscular Junction; Peptide Hydrolases; Rana pipiens

1985