Injury-induced functional plasticity in the peripheral gustatory system.

Combining unilateral denervation of anterior tongue taste buds with a low-sodium diet in rats results in a rapid, dramatic, and selective attenuation of neurophysiological sodium taste responses from the intact side of the tongue. The transduction pathway responsible for the attenuated response is through the epithelial sodium channel (Hill and Phillips, 1994). Current experiments extend these findings by detailing the effects of experimentally induced injury on taste responses from anterior tongue taste receptors in sodium-restricted rats. Experiments focused on functional salt taste responses from the intact chorda tympani nerve in sodium-restricted rats in which a gustatory nerve was sectioned that innervates the anterior tongue (chorda tympani), the posterior tongue (glossopharyngeal), or palatal taste receptors (greater superficial petrosal) or in which a nongustatory nerve was sectioned that also has its target in the anterior tongue (trigeminal). An additional group was studied that received thermal injury to the anteroventral tongue. Substantial and selective suppression of sodium salt responses occurred in a graded manner generally related to the distance from the target field of the injury to anterior tongue taste buds. The order of effectiveness was: chorda tympani section > trigeminal section > thermal injury = glossopharyngeal section > greater superficial petrosal section. These results support the hypothesis that local, diffusible factors liberated from immune-derived cells as a result of neural and/or epithelial damage are involved in regulating the transduction pathway responsible for sodium salt sensation, and that these factors may become evident through dietary sodium restriction.