The impact of vitamin C on diabetes induced alterations at murine neuromuscular junction

Physiological functions of skeletal muscle are compromised in diabetes. This may involve free radical mechanisms and may be reversed by antioxidants. We have studied effects of vitamin C on twitch tension, resting membrane potential (RMP) and miniature endplate potentials (MEPPs) frequencies in dorsiflexor muscle of diabetic murine. Forty mice were divided randomly into 2 groups (n = 20 each). One group served as control and the other was injected once with streptozotocin (STZ) solution (60 mg/kg, i.p) to induce diabetes. The animals were then divided further into two subgroups (n = 10 each). Vitamin C (200 mg/kg, i.p) was administered daily to one control and one diabetic group for three weeks prior to recording day. Experiments were conducted four weeks following diabetes induction. Isometric twitch tension (evoked directly by muscle stimulation and indirectly by nerve stimulation) was measured in urethane anesthetized (2 mg/g, i.p) mice via a transducer connected to computer system. Utilizing intracellular recording method, resting membrane potential RMP and MEPPs frequencies were also measured. Compared to control, diabetic mice showed reduced twitch tension (4.2 ± 0.5 g control versus 2.6 ± 0.2 g diabetic) and demonstrated delayed half time of decay. Diabetic flexor muscle also displayed significant reduction in MEPPs frequencies with no changes in RMP. Vitamin C reversed tension reduction in diabetic mice (from 2.6 ± 0.2 g to 3.9 ± 0.3 g), impacted delayed half time of decay and increased MEPPs frequencies. Vitamin C improves diabetes-induced nerve and muscle dysfunction possibly via a free radical scavenging mechanism.