Abstract
The antinociceptive effect of mexiletine in diabetic mice was examined.Tail−flick latencies at heat intensity of 35 and 50 V in diabetic mice were shorter than those in non−diabetic mice.In diabetic mice, mexiletine increased the tail−flick latency at 35 V to the level observed in non−diabetic mice.The tail−flick latency at 50 V in diabetic mice, but not in non−diabetic mice, was increased by pretreatment with capsaicin(0.56 nmol, i.t., 24 h).The antinociceptive effect of mexiletine in diabetic mice was reduced by capsaicin.These results suggest that the mexiletine−induced antinociception in diabetic mice involves the inhibition of the nociceptive transmission of capsaicin−sensitive primary afferent fibers.
