ABSTRACT
BACKGROUND: Allodynia, one of the most debilitating symptoms of neuropathic pain syndromes, can be defined as `pain due to a stimulus that does not normally provoke pain'. Subsets of dorsal root ganglion (DRG) neurons involved in nociception are characteristically expressed capsaicin sensitivity and high proportion of tetrodotoxin resistant sodium current (TTX-R INa). We performed an experiment to elucidate whether nerve injury induced mechanical allodynia could be resulted from elctrophysiological modulation of large, nonnociceptive afferent neurons to nociceptors. METHODS: Whole cell patch clamp recordings were made from acutely dissociated dorsal root ganglion (DRG) neurons of normal and experimental neuropathic rats. We compared the proportion of capsaicin sensitive neurons which responded to capsaicin (1micrometer) with an inward current > or = 100 pA in amplitude and the proportion of sodium channel subtypes measured in the absence and presence of tetrodotoxin (1micrometer), in small and large DRG neurons. RESULTS: The proportion of capsaicin sensitive cells to total number of cells tested was not changed by nerve injury in both small and large cell populations. In large cell population of nerve injured rats, the proportion of TTX-R INa was significantly increased as compared with normal group (p <0.05), and in small cell population of nerve injured rats, TTX-S INa was increased, but there was no statistical significance. CONCLUSIONS: These data indicate that expression of the sensitivity to capsaicin in DRG neurons would not be altered by nerve injury and increased TTX-R INa in large cell population of nerve injured DRG may underlie increased excitability.