Human clinical and psychophysical observations suggest that the taste syste
m is able to compensate for losses in peripheral nerve input, since patient
s do not commonly report decrements in whole mouth taste following chorda t
ympani nerve damage or anesthesia. Indeed, neurophysiological data from the
rat nucleus of the solitary tract (NST) suggests that a release of inhibit
ion (disinhibition) may occur centrally following chorda tympani nerve anes
thesia. Our purpose was to study this possibility further. We recorded from
59 multi- and single-unit taste-responsive sites in the rat NST before, du
ring and after recovery from chorda tympani nerve anesthesia. During anesth
esia, 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 anest
hesia. The average increase was 32.9%. Therefore, disinhibition of taste re
sponses was observed, but infrequently and to a small degree in the NST. At
a subset of sites, chorda tympani-mediated responses decreased while greate
r superficial petrosal-mediated responses remained the same during anesthes
ia. Since this effect was accompanied by a decrease in spontaneous activity
, we propose that taste compensation may result in part by a change in sign
al-to-noise ratio at a subset of sites.