Capsaicin is a key molecule in neuropathic pain induced by diabetes

Diabetic peripheral neuropathy is a common chronic complica-tion of diabetes mellitus. Transient receptor potential (TRP) ion channels are involved in sensing physical and chemical stimuli.TRPV1 is a Ca2+ permeant non-selective cation channel expressed predominantly by unmyelinated C-fibers and thinly myelinated A-delta fibers and plays a major role in inflammatory thermal sensation. Capsaicin is the active component of chili peppers (which are plants belonging to the genus Capsicum) and is the main compound responsible for TRPV1 activation. In this study, we have used a transgene-mediated diabetes model to study the role of capsaicin in diabetic peripheral neuropathy. We have used sensory neurons from dorsal root ganglia prelevated from TCR-HA+/)/Ins-HA+/- mice and Balb/c mice. Whole cell patch-clamp recording and immunofluorescence microscopy have been employed. The larger amplitude and reduced desensitization of TRPV1 currents induced by capsaicin, obtained in TCR-HA+/)/Ins-HA+/- mice, closely resemble changes identified in streptozotocin-induced diabetes in rats. Expression of TRPV1 was significantly higher in the double-transgenic diabetic mice. Capsaicin treatment reduced the TRPV1 expression. In diabetes, the link between abnormal pain sensitivity and hyperglycemia resulting from insulin deficiency is not clear, but our study proves that capsaicin plays a major role in regulating TRPV1 functional expression in diabetes. This study was financed by the research grant PNCDI2 41-074/2007