Salt taste discrimination after bilateral section of the chorda tympani or glossopharyngeal nerves

1992 ◽  
Vol 263 (1) ◽  
pp. R169-R176 ◽  
Author(s):  
A. C. Spector ◽  
H. J. Grill

Gustatory deafferentation of the anterior tongue by bilateral section of the chorda tympani nerve, which removes only 15% of the total taste buds in the rat, severely impaired the rat's ability to discriminate NaCl from KCl. The discrimination deficit was selective. Denervated rats were able to discriminate sucrose from quinine. Despite eliminating four times as many taste buds by bilateral section of the glossopharyngeal nerve, posterior lingual deafferentation had no effect on NaCl vs. KCl discrimination performance. Collectively, these data suggest that afferents in the chorda tympani nerve provide the highest degree of disparity between the peripheral signals representing NaCl and KCl. Electrophysiological findings of others implicate the sodium-specific afferents that appear to exclusively exist in the chorda tympani nerve as the critical elements subserving the NaCl vs. KCl discrimination.

2000 ◽  
Vol 278 (3) ◽  
pp. R720-R731 ◽  
Author(s):  
Stacy L. Kopka ◽  
Laura C. Geran ◽  
Alan C. Spector

We tested whether the recovered ability of rats to discriminate NaCl from KCl after chorda tympani nerve transection (CTX) is causally linked to nerve regeneration or some other compensatory process. Rats were presurgically trained in an operant NaCl vs. KCl discrimination task. Rats with regenerated nerves, histologically confirmed by anterior tongue taste pore counts and tested 62 days after CTX (CTX-62R; n = 5), performed as well as those tested 62 days after sham surgery (Sham-62; n = 5), but both of these groups initially performed slightly worse than animals tested 7 days after sham surgery (Sham-7; n = 4). Performance of rats tested either 7 (CTX-7P; n = 5) or 62 (CTX-62P; n = 4) days after CTX in which nerve regeneration was prevented was severely disrupted. Adulteration of the stimuli with amiloride, an epithelial sodium channel blocker, impaired discrimination performance in a similar dose-dependent manner in the Sham-7 ( n = 2), Sham-62 ( n = 5), and CTX-62R ( n = 5) groups, suggesting that the functional status of the amiloride-sensitive transduction pathway returns to normal in rats with regenerated chorda tympani nerves. Performance of CTX rats without regenerated nerves (CTX-7P, n = 2; CTX-62P, n = 4) was further degraded by amiloride treatment, suggesting that taste receptors innervated by other nerves are sensitive to amiloride. In conclusion, nerve regeneration is an essential component underlying full recovery of salt discrimination function after CTX.


1995 ◽  
Vol 269 (1) ◽  
pp. R141-R153 ◽  
Author(s):  
S. J. St John ◽  
S. Markison ◽  
A. C. Spector

Transection of the chorda tympani nerve (CTX) impairs taste-guided discrimination of NaCl from KCl in rats. We wanted to determine whether this discrimination recovers after chorda tympani regeneration. Experiment 1 showed that few taste buds regenerated 14 days after CTX, whereas substantial regeneration occurred 42 days after surgery. Experiment 2 demonstrated that rats trained before CTX could clearly discriminate the two salts when tested starting 49 days after surgery, whereas rats tested starting 8 days after surgery were severely impaired in this task. Rats tested starting 28 days after CTX were unimpaired, moderately impaired, or severely impaired on the discrimination task. Overall, discrimination performance was significantly related to the number of regenerated taste buds. Unilaterally transected rats tested shortly after surgery were nearly as competent as controls. These results indicate that rats can recover the ability to discriminate NaCl from KCl after regeneration of anterior tongue taste buds.


2010 ◽  
Vol 299 (4) ◽  
pp. R1027-R1036 ◽  
Author(s):  
Ginger Blonde ◽  
Enshe Jiang ◽  
Mircea Garcea ◽  
Alan C. Spector

Rats lacking input to the chorda tympani (CT) nerve, a facial nerve branch innervating anterior tongue taste buds, show robust impairments in salt discrimination demonstrating its necessity. We tested the sufficiency of the CT for salt taste discrimination and whether the remaining input provided by the greater superficial petrosal (GSP) nerve, a facial nerve branch innervating palatal taste buds, or by the glossopharyngeal (GL) nerve, innervating posterior tongue taste buds, could support performance after extended postsurgical testing. Rats presurgically trained and tested in a two-response operant task to discriminate NaCl from KCl were subjected to sham surgery or transection of the CT (CTx), GL (GLx), or GSP (GSPx), alone or in combination. While initially reduced postsurgically, performance by rats with an intact GSP after CTx + GLx increased to normal over 6 wk of testing. Rats with CTx + GSPx consistently performed near chance levels. In contrast, rats with GSPx + GLx were behaviorally normal. A subset of rats subjected to sham surgery and exposed to lower concentrations during postsurgical testing emulating decreased stimulus intensity after neurotomy showed no significant impairment. These results demonstrate that CTx changes the perceptual nature of NaCl and/or KCl, leading to severe initial postsurgical impairments in discriminability, but a “new” discrimination can be relearned based on the input of the GSP. Despite losing ∼75% of their taste buds, rats are unaffected after GSPx + GLx, demonstrating that the CT is not only necessary, but also sufficient, for maintaining salt taste discrimination, notwithstanding the unlikely contribution of the small percentage of taste receptors innervated by the superior laryngeal nerve.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.


2015 ◽  
Vol 10 (6) ◽  
pp. 989 ◽  
Author(s):  
Dong-dong Ren ◽  
Fang-lu Chi ◽  
Yi-ke Li ◽  
Juan-mei Yang ◽  
Yi-bo Huang

1994 ◽  
Vol 104 (5) ◽  
pp. 885-907 ◽  
Author(s):  
Q Ye ◽  
G L Heck ◽  
J A DeSimone

Taste sensory responses from the chorda tympani nerve of the rat were recorded with the lingual receptive field under current or voltage clamp. Consistent with previous results (Ye, Q., G. L. Heck, and J. A. DeSimone. 1993. Journal of Neurophysiology. 70:167-178), responses to NaCl were highly sensitive to lingual voltage clamp condition. This can be attributed to changes in the electrochemical driving force for Na+ ions through apical membrane transducer channels in taste cells. In contrast, responses to KCl over the concentration range 50-500 mM were insensitive to the voltage clamp condition of the receptive field. These results indicate the absence of K+ conductances comparable to those for Na+ in the apical membranes of taste cells. This was supported by the strong anion dependence of K salt responses. At zero current clamp, the potassium gluconate (KGlu) threshold was > 250 mM, and onset kinetics were slow (12 s to reach half-maximal response). Faster onset kinetics and larger responses to KGlu occurred at negative voltage clamp (-50 mV). This indicates that when K+ ion is transported as a current, and thereby uncoupled from gluconate mobility, its rate of delivery to the K+ taste transducer increases. Analysis of conductances shows that the paracellular pathway in the lingual epithelium is 28 times more permeable to KCl than to KGlu. Responses to KGlu under negative voltage clamp were not affected by agents that are K+ channel blockers in other systems. The results indicate that K salt taste transduction is under paracellular diffusion control, which limits chemoreception efficiency. We conclude that rat K salt taste occurs by means of a subtight junctional transducer for K+ ions with access limited by anion mobility. The data suggest that this transducer is not cation selective which also accounts for the voltage and amiloride insensitive part of the response to NaCl.


1994 ◽  
Vol 266 (5) ◽  
pp. C1165-C1172 ◽  
Author(s):  
A. M. Feigin ◽  
Y. Ninomiya ◽  
S. M. Bezrukov ◽  
B. P. Bryant ◽  
P. A. Moore ◽  
...  

Single fibers of the rat chorda tympani nerve were used to study the mechanism of action of the antibiotic novobiocin on salt taste transduction. In the rat, novobiocin selectively enhanced the responses of sodium-specific and amiloride-sensitive chorda tympani nerve fibers (N type) without affecting more broadly responsive cation-sensitive and amiloride-insensitive fibers (E type). In the presence of amiloride, novobiocin was ineffective at enhancing the response of N-type fibers toward sodium chloride. Novobiocin also increased the conductance of bilayers formed from neutral lipids by forming nonrectifying ion channels with low conductance (approximately 7 pS in 110 mM NaCl), long open times (several seconds and longer), and high cation selectivity. Amiloride did not alter either the conductance or kinetics of these novobiocin channels. These observations suggest that even though novobiocin is able to form cation channels in lipid bilayers, and possibly in cell membranes as well, its action on the salt-taste response is through modulation of existing amiloride-sensitive sodium channels.


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