AI Article Synopsis

  • Research shows that rerouting gustatory nerves in the tongue can lead to the partial recovery of taste functions, especially when the correct taste field is targeted.
  • When the bitter-responsive posterior tongue was connected to the chorda tympani nerve, some oromotor reflexes and neural activity were restored, unlike when the anterior tongue was connected to the glossopharyngeal nerve.
  • The study also found specific brain areas related to bitter taste, like the central nucleus of the amygdala and gustatory cortex, showcased changes in neuron activity that correlate with the reflexive responses to quinine, highlighting the system's adaptability and the importance of correct nerve-field connections.

Article Abstract

Remarkably, when lingual gustatory nerves are surgically rerouted to inappropriate taste fields in the tongue, some taste functions recover. We previously demonstrated that quinine-stimulated oromotor rejection reflexes and neural activity (assessed by Fos immunoreactivity) in subregions of hindbrain gustatory nuclei were restored if the posterior tongue, which contains receptor cells that respond strongly to bitter compounds, was cross-reinnervated by the chorda tympani nerve. Such functional recovery was not seen if instead, the anterior tongue, where receptor cells are less responsive to bitter compounds, was cross-reinnervated by the glossopharyngeal nerve, even though this nerve typically responds robustly to bitter substances. Thus, recovery depended more on the taste field being reinnervated than on the nerve itself. Here, the distribution of quinine-stimulated Fos-immunoreactive neurons in two taste-associated forebrain areas was examined in these same rats. In the central nucleus of the amygdala (CeA), a rostrocaudal gradient characterized the normal quinine-stimulated Fos response, with the greatest number of labeled cells situated rostrally. Quinine-stimulated neurons were found throughout the gustatory cortex, but a "hot spot" was observed in its anterior-posterior center in subregions approximating the dysgranular/agranular layers. Fos neurons here and in the rostral CeA were highly correlated with quinine-elicited gapes. Denervation of the posterior tongue eliminated, and its reinnervation by either nerve restored, numbers of quinine-stimulated labeled cells in the rostralmost CeA and in the subregion approximating the dysgranular gustatory cortex. These results underscore the remarkable plasticity of the gustatory system and also help clarify the functional anatomy of neural circuits activated by bitter taste stimulation.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157664PMC
http://dx.doi.org/10.1002/cne.23546DOI Listing

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