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Human clinical and psychophysical observations suggest that the taste
system is able to compensate for losses in peripheral nerve input, since
patients do not commonly report decrements in whole mouth taste following
chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data
from the rat nucleus of the solitary tract (NST) suggests that a release of
inhibition (disinhibition) may occur centrally following chorda tympani
nerve anesthesia. Our purpose was to study this possibility further. We
recorded from 59 multi- and single- unit taste-responsive sites in the rat
NST before, during and after recovery from chorda tympani nerve anesthesia.
During anesthesia, average anterior tongue responses were eliminated but no
compensatory increases in palatal or posterior tongue responses were
observed. However, six individual sites displayed increased taste
responsiveness during anesthesia. The average increase was 32.9%.
Therefore, disinhibition of taste responses was observed, but infrequently
and to a small degree in the NST At a subset of sites, chorda
tympani-mediated responses decreased while greater superficial
petrosal-mediated responses remained the same during anesthesia. Since this
effect was accompanied by a decrease in spontaneous activity, we propose
that taste compensation may result in part by a change in signal-to-noise
ratio at a subset of sites.
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