Cobalt Affects Neuromuscular Transmission of Diabetic Mice

Skeletal muscle function is compromised in diabetes and Ca2+ mobilization is suspected as a mechanism. Cobalt affects Ca2+ receptors at motor nerve terminals. We investigated effects of cobalt on diabetic neuromuscular transmission. Twenty C57BL mice (28.7 + 0.9 g) were divided randomly into 2 groups. One group (n=10) served as control and the other (n=10) were injected once with (streptozotocin) STZ (60 mg/kg, i.p) to induce diabetes. Resting membrane potential, spontaneous miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) were measured intracellularly in urethane‐anaesthetized (2 mg/g, i.p) control and four weeks diabetic mice following administration of 5 mM cobalt. Results were analyzed statistically using ANOVA. In control mice, exposure of the flexor muscle to 5 mM cobalt for 10 min did not change both resting membrane potential and MEPPs frequency and amplitude. In reduced Ca2+ high Mg2+ addition of 5 mM cobalt reduced EPPs amplitude to 25% of its control value (p<0.05). In STZ‐diabetic mice 5 mM cobalt did not change resting membrane and MEPPs amplitude but raised MEPPs frequency by 100% (p<0.001) and reduced EPPs amplitude to 50% as compared with control values (p<0.01). Less inhibition of EPPs by cobalt in diabetic than in control mice confirms the action of cobalt on neuromuscular junction and suggests that altered intracellular Ca2+ may be involved in diabetic neuromyopathy.