Transganglionic degeneration in the gustatory system consequent to chorda tympani damage.

The chorda tympani taste nerve is prone to damage in humans. Chorda tympani damage results in taste loss accompanied by altered taste sensations, e.g., phantom tastes. To understand taste alterations this study explores the central and peripheral anatomical consequences of taste nerve injury in an animal model. The chorda tympani was severed in the middle ear of hamsters and the animals were allowed to survive for 2-161 days when sections of the brain were stained for degenerating axons with the Fink-Heimer method. Degenerating axons were present in the chorda tympani termination zone in the nucleus of the solitary tract of every case. Thus, peripheral nerve damage in the taste system results in degeneration of central axonal endings as in other sensory systems (e.g., trigeminal, vestibular). To evaluate whether the central degeneration results from ganglion cell death, geniculate ganglion cells were labeled with Fast blue by tongue injections before neurotomy, and the cells were counted 13-48 days after neurotomy. Numbers of labeled cells from experimental ganglia did not differ significantly from those in control ganglia. Moreover, the experimental cells could be double-labeled by tongue injections with a second marker, diamidino yellow or nuclear yellow, after 40 days postneurotomy. We conclude that degeneration of central axons after taste nerve section represents a long-lasting transganglionic process that likely disrupts the synaptology of the central taste system. The altered synaptology could relate to taste phenomena of central origin reported for nerve-injured patients. Geniculate ganglion cells generally survive neurotomy and can regenerate axons to the tongue.