scholarly journals Effects of voltage perturbation of the lingual receptive field on chorda tympani responses to Na+ and K+ salts in the rat: implications for gustatory transduction.

1994 ◽  
Vol 104 (5) ◽  
pp. 885-907 ◽  
Author(s):  
Q Ye ◽  
G L Heck ◽  
J A DeSimone
Keyword(s):  
Receptive Field ◽  
Voltage Clamp ◽  
Maximal Response ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Negative Voltage ◽  
Voltage Clamp Condition ◽  
Taste Cells ◽  
Clamp Condition

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.

Chorda tympani taste response of rat to hydrochloric acid subject to voltage-clamped lingual receptive field

1995 ◽  
Vol 268 (5) ◽  
pp. C1295-C1300 ◽  
Author(s):  
J. A. DeSimone ◽  
E. M. Callaham ◽  
G. L. Heck
Keyword(s):  
Receptive Field ◽  
Voltage Clamp ◽  
Paracellular Pathway ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Anionic Sites ◽  
Taste Response ◽  
Nerve Response ◽  
Zero Current ◽  
Positive Voltage

The chorda tympani nerve response of the rat to HCl was obtained with the lingual receptive field under voltage clamp. Unlike NaCl responses, HCl responses were not affected by inside positive voltage perturbations. However, HCl responses under negative voltage clamp were suppressed in contrast to NaCl responses, which were enhanced. Unlike NaCl responses, HCl responses were amiloride insensitive. HCl rinsing from the tongue produced a large off-response. At zero current clamp the off-response coincided with an anomalous increased positive potential. The paracellular resistance was also higher for HCl relative to the same concentration of NaCl. This is evidence that H+ binds to the normally fixed anionic sites of the paracellular pathway rendering it anion selective. It is postulated that release of bound H+ from surface buffer sites is responsible for the second burst of neural activity upon rising HCl. Acids stimulate primarily through the paracellular pathway, which also furnishes buffering sites that regulate H+ concentration, thereby protecting the sensory apparatus from hyperacidic conditions.

scholarly journals Relation of Receptive Field Size and Salt Taste Responses in Chorda Tympani Fibers during Development

1987 ◽  
Vol 510 (1 Olfaction and) ◽  
pp. 504-505
Author(s):  
CHARLOTTE M. MISTRETTA ◽  
TAKATOSHI NAGAI ◽  
ROBERT M. BRADLEY
Keyword(s):  
Receptive Field ◽  
Field Size ◽  
Chorda Tympani ◽  
Receptive Field Size ◽  
Salt Taste

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
Keyword(s):  
Discrimination Performance ◽  
Taste Buds ◽  
Glossopharyngeal Nerve ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Critical Elements ◽  
Electrophysiological Findings ◽  
Taste Discrimination ◽  
Salt Taste Discrimination

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.

scholarly journals Optogenetic Activation of Type III Taste Cells Modulates Taste Responses

2020 ◽  
Vol 45 (7) ◽  
pp. 533-539
Author(s):  
Aurelie Vandenbeuch ◽  
Courtney E Wilson ◽  
Sue C Kinnamon
Keyword(s):  
Light Response ◽  
Sensory Nerves ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Type Iii ◽  
Nonspecific Effects ◽  
Taste Cells ◽  
Specific Stimulation ◽  
The Brain

Abstract Studies have suggested that communication between taste cells shapes the gustatory signal before transmission to the brain. To further explore the possibility of intragemmal signal modulation, we adopted an optogenetic approach to stimulate sour-sensitive (Type III) taste cells using mice expressing Cre recombinase under a specific Type III cell promoter, Pkd2l1 (polycystic kidney disease-2-like 1), crossed with mice expressing Cre-dependent channelrhodopsin (ChR2). The application of blue light onto the tongue allowed for the specific stimulation of Type III cells and circumvented the nonspecific effects of chemical stimulation. To understand whether taste modality information is preprocessed in the taste bud before transmission to the sensory nerves, we recorded chorda tympani nerve activity during light and/or chemical tastant application to the tongue. To assess intragemmal modulation, we compared nerve responses to various tastants with or without concurrent light-induced activation of the Type III cells. Our results show that light significantly decreased taste responses to sweet, bitter, salty, and acidic stimuli. On the contrary, the light response was not consistently affected by sweet or bitter stimuli, suggesting that activation of Type II cells does not affect nerve responses to stimuli that activate Type III cells.

Sweet Taste Responses of Mouse Chorda Tympani Neurons: Existence of Gurmarin-Sensitive and -Insensitive Receptor Components

1999 ◽  
Vol 81 (6) ◽  
pp. 3087-3091 ◽  
Author(s):  
Yuzo Ninomiya ◽  
Toshiaki Imoto ◽  
Tadataka Sugimura
Keyword(s):  
Sweet Taste ◽  
The Other ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Inhibitory Effects ◽  
Single Fibers ◽  
Taste Cells ◽  
C57bl Mice ◽  
Mouse Taste

Sweet taste responses of mouse chorda tympani neurons: existence of gurmarin-sensitive and -insensitive receptor components. Inhibitory effects of gurmarin (gur) on responses to sucrose and other sweeteners of single fibers of the chorda tympani nerve in C57BL mice were examined. Of 30 single fibers that strongly responded to 0.5 M sucrose but were not or to lesser extent responsive to 0.1 M NaCl, 0.01 M HCl, and 0.02 M quinine HCl (sucrose-best fibers), 16 fibers showed large suppression of responses to sucrose and other sweeteners by lingual treatment with 4.8 μM (∼20 μg/ml) gur (suppressed to 4–52% of control: gur-sensitive fibers), whereas the remaining 14 fibers showed no such gur inhibition (77–106% of control: gur-insensitive fibers). In gur-sensitive fibers, responses to sucrose inhibited by gur recovered to ∼70% of control responses after rinsing the tongue with 15 mM β-cyclodextrin and were almost abolished by further treatment with 2% pronase. In gur-insensitive fibers, sucrose responses were not inhibited by gur, but were largely suppressed by pronase. These results suggest existence of two different receptor components for sweeteners with different susceptibilities to gur in mouse taste cells, one gur sensitive and the other gur insensitive. Taste cells possessing each component may be specifically innervated by a particular type of chorda tympani neurons.

scholarly journals Acetic acid modulates spike rate and spike latency to salt in peripheral gustatory neurons of rats

2012 ◽  
Vol 108 (9) ◽  
pp. 2405-2418 ◽  
Author(s):  
Joseph M. Breza ◽  
Robert J. Contreras
Keyword(s):  
Acetic Acid ◽  
Artificial Saliva ◽  
Type I ◽  
Dependent Manner ◽  
Chorda Tympani ◽  
Gustatory System ◽  
Chorda Tympani Nerve ◽  
Concentration Dependent Manner ◽  
Lingual Epithelium ◽  
Taste Cells

Sour and salt taste interactions are not well understood in the peripheral gustatory system. Therefore, we investigated the interaction of acetic acid and NaCl on taste processing by rat chorda tympani neurons. We recorded multi-unit responses from the severed chorda tympani nerve (CT) and single-cell responses from intact narrowly tuned and broadly tuned salt-sensitive neurons in the geniculate ganglion simultaneously with stimulus-evoked summated potentials to signal when the stimulus contacted the lingual epithelium. Artificial saliva served as the rinse and solvent for all stimuli [0.3 M NH4Cl, 0.5 M sucrose, 0.1 M NaCl, 0.01 M citric acid, 0.02 M quinine hydrochloride (QHCl), 0.1 M KCl, 0.003–0.1 M acetic acid, and 0.003–0.1 M acetic acid mixed with 0.1 M NaCl]. We used benzamil to assess NaCl responses mediated by the epithelial sodium channel (ENaC). The CT nerve responses to acetic acid/NaCl mixtures were less than those predicted by summing the component responses. Single-unit analyses revealed that acetic acid activated acid-generalist neurons exclusively in a concentration-dependent manner: increasing acid concentration increased response frequency and decreased response latency in a parallel fashion. Acetic acid suppressed NaCl responses in ENaC-dependent NaCl-specialist neurons, whereas acetic acid-NaCl mixtures were additive in acid-generalist neurons. These data suggest that acetic acid attenuates sodium responses in ENaC-expressing-taste cells in contact with NaCl-specialist neurons, whereas acetic acid-NaCl mixtures activate distinct receptor/cellular mechanisms on taste cells in contact with acid-generalist neurons. We speculate that NaCl-specialist neurons are in contact with type I cells, whereas acid-generalist neurons are in contact with type III cells in fungiform taste buds.

Enhancement of gustatory nerve fibers to NaCl and formation of ion channels by commercial novobiocin

1994 ◽  
Vol 266 (5) ◽  
pp. C1165-C1172 ◽  
Author(s):  
A. M. Feigin ◽  
Y. Ninomiya ◽  
S. M. Bezrukov ◽  
B. P. Bryant ◽  
P. A. Moore ◽  
...  
Keyword(s):  
Ion Channels ◽  
Lipid Bilayers ◽  
Neutral Lipids ◽  
Nerve Fibers ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Cation Selectivity ◽  
Taste Response ◽  
Gustatory Nerve

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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