Ultrastructural localization of calcium in neuromuscular junctions of smooth and skeletal muscles after aminoglycoside antibiotics treatment

Abstract

Aminoglycoside antibiotics are all capable of producing clinically significant neuromuscular paralysis. Since part of the mechanism of action of these antibiotics at neuromuscular junction is a calciumdependent inhibition of acetylcholine release, so this experiment was carried out in vitro on both somatic (isolated rat phrenic-nerve hemidiaphragm) and autonomic neuro-effector transmission (guinea-pig ileum) using gentamicin and amikacin, to determine the calcium contents at this level. Electron microscopic observations on gentamycinandlor amikacin-treated materials, using potassium pyroantimonate method suggest a reduction of internal calcium in nerve terminals of both preparations.