Physiological effects of caffeine on neuromuscular transmission in streptozotocin induced diabetes

The flexor digitorum superficialis muscle of C57BL mice was selected to study the effects of caffeine on membrane potentials, spontaneous transmitter release, muscle twitch tension and synaptic delay in diabetes mellitus. Twenty mice were injected once with streptozotocin (STZ) solution (60 mg/kg, i.p.) to induce diabetes and another twenty served as controls. Resting Membrane Potential (RMP) and miniature endplate potentials (MEPPs) were recorded following administration of 5 mM caffeine at various K⁺ concentrations (5, 10, 15, 20 mM). Isometric contractile activities (at 1, 5 and 30 Hz stimulation via nerve or muscle) were also measured after giving 5 mM caffeine. Following caffeine treatment MEPPs frequencies were increased in control group. MEPPs frequencies became reduced with diabetes and adding caffeine caused a significant increase that went above normal values. High K⁺ concentration also augmented the effect of caffeine on RMP and MEPPs. Diabetic groups generated less twitch tension compared to control and had prolonged synaptic latencies. Adding caffeine caused increase in twitch tensions in both groups. This modification mostly occurred in diabetic group and was more pronounced when tension was originated via indirect nerve stimulation of muscle. Current results indicate that the modulatory effects of caffeine on diabetic neuromyopathy may probably result from altering Ca²⁺ mobilization in nerve or muscle.