Effects of cross-wiring the lingual taste nerves on quinine-stimulated Fos-immunoreactivity in the rat parabrachial nucleus.

Abstract

By surgically cross-wiring the taste nerves into non-native receptor fields (the glossopharyngeal (GL) into the anterior tongue (GLc/AT) or the chorda tympani (CT) into the posterior tongue (CTc/PT)), we showed previously that unconditioned quinine-induced gaping and neuronal activity, assessed by c-Fos immunohistochemistry, in the rostral nucleus of the solitary tract (rNST), were fully and partially restored, respectively, only if the PT taste receptor field was reinnervated; the particular taste nerve supplying the input was inconsequential to the recovery of function. These findings suggested that a cluster of Fos-expressing cells in the most rostral pole of the rNST may be importantly associated with neural circuits involved in the generation of unconditioned taste-triggered rejection reflexes. We are now examining in these same animals the distribution of Fos-positive neurons in the waist area of the parabrachial nucleus (PBN), the second obligatory central relay in the ascending rodent gustatory system. Preliminary data indicate that quinine-stimulated controls (N=3) and animals with regeneration of the GL into its native PT receptor field (N=2) show robust neural activity (121.0±33.5 and 136.5±6.5 Fos-positive neurons, respectively) compared with water-stimulated controls (N=3, 31.6±6.1). The CTc/PT cross-wiring (N=3) appears to be more effective in maintaining quinine-stimulated neural activity in the waist area (81.3±18.0) than the GLc/AT cross-wiring (N=3, 30.0±8.6). Presently, we are analyzing the remaining subjects and other PBN subdivisions to explore further the remarkable ability of the central gustatory to adapt to peripherally reorganized neural taste input. Supported by NIH-R01-DC01628.