The purpose of this study was to investigate the role of response latency in discrimination of chemical stimuli by geniculate ganglion neurons in the rat. Accordingly, we recorded single-cell 5-s responses from geniculate ganglion neurons (n = 47) simultaneously with stimulus-evoked summated potentials (electrogustogram; EGG) from the anterior tongue to signal when the stimulus contacted the lingual epithelium. Artificial saliva served as the rinse solution and solvent for all stimuli [(0.5 M sucrose, 0.03-0.5 M NaCl, 0.01 M citric acid, and 0.02 M quinine hydrochloride (QHCl)], 0.1 M KCl as well as for 0.1 M NaCl +1 μM benzamil. Cluster analysis separated neurons into four groups (sucrose specialists, NaCl specialists, NaCl/QHCl generalists and acid generalists). Artificial saliva elevated spontaneous firing rate and response frequency of all neurons. As a rule, geniculate ganglion neurons responded with the highest frequency and shortest latency to their best stimulus with acid generalist the only exception. For specialist neurons and NaCl/QHCl generalists, the average response latency to the best stimulus was two to four times shorter than the latency to secondary stimuli. For NaCl-specialist neurons, response frequency increased and response latency decreased systematically with increasing NaCl concentration; benzamil significantly decreased NaCl response frequency and increased response latency. Acid-generalist neurons had the highest spontaneous firing rate and were the only group that responded consistently to citric acid and KCl. For many acid generalists, a citric-acid-evoked inhibition preceded robust excitation. We conclude that response latency may be an informative coding signal for peripheral chemosensory neurons.

In humans, temperature influences taste intensity and quality perception, and thermal stimulation itself may elicit taste sensations. However, peripheral coding mechanisms of taste have generally been examined independently of the influence of temperature. In anesthetized rats, we characterized the single-cell responses of geniculate ganglion neurons to 0.5 M sucrose, 0.1 M NaCl, 0.01 M citric acid, and 0.02 M quinine hydrochloride at a steady, baseline temperature (adapted) of 10, 25, and 40 degrees C; gradual cooling and warming (1 degrees C/s change in water temperature >5 s) from an adapted tongue temperature of 25 degrees C; gradual cooling from an adapted temperature of 40 degrees C; and gradual warming from an adapted temperature of 10 degrees C. Hierarchical cluster analysis of the taste responses at 25 degrees C divided 50 neurons into two major categories of narrowly tuned (Sucrose-specialists, NaCl-specialists) and broadly tuned (NaCl-generalists(I), NaCl- generalists(II), Acid-generalists, and QHCl-generalists) groups. NaCl specialists were excited by cooling from 25 to 10 degrees C and inhibited by warming from 10 to 25 degrees C. Acid-generalists were excited by cooling from 40 to 25 degrees C but not from 25 to 10 degrees C. In general, the taste responses of broadly tuned neurons decreased systematically to all stimuli with decreasing adapted temperatures. The response selectivity of Sucrose-specialists for sucrose and NaCl-specialists for NaCl was unaffected by adapted temperature. However, Sucrose-specialists were unresponsive to sucrose at 10 degrees C, whereas NaCl-specialists responded equally to NaCl at all adapted temperatures. In conclusion, we have shown that temperature modulates taste responsiveness and is itself a stimulus for activation in specific types of peripheral gustatory neurons.

Breza JM, Contreras RJ. Anion size modulates salt taste in rats. J Neurophysiol 107: 1632-1648, 2012. First published December 28, 2011 doi:10.1152/jn.00621.2011.-The purpose of this study was to investigate the influence of anion size and the contribution of the epithelial sodium channel (ENaC) and the transient receptor potential vanilloid-1 (TRPV1) channel on sodium-taste responses in rat chorda tympani (CT) neurons. We recorded multiunit responses from the severed CT nerve 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 NH 4 Cl, 0.5 M sucrose, 0.03-0.5 M NaCl, 0.01 M citric acid, 0.02 M quinine hydrochloride, 0.1 M KCl, and 0.03-0.5 M Na-gluconate). We used the pharmacological antagonist benzamil to assess NaCl responses mediated by ENaC, and SB-366791 and cetylpyridinium chloride to assess responses mediated by TRPV1. CT nerve responses were greater to NaCl than Na-gluconate at each concentration; this was attributed mostly to broadly tuned, acid-generalist neurons that responded with higher frequency and shorter latency to NaCl than Na-gluconate. In contrast, narrowly tuned NaCl-specialist neurons responded more similarly to the two salts, but with subtle differences in temporal pattern. Benzamil reduced CT nerve and single-cell responses only of narrowly tuned neurons to NaCl. Surprisingly, SB-366791 and cetylpyridinium chloride were without effect on CT nerve or single-cell NaCl responses. Collectively, our data demonstrate the critical role that apical ENaCs in fungiform papillae play in processing information about sodium by peripheral gustatory neurons; the role of TRPV1 channels is an enigma. chorda tympani; geniculate ganglion; epithelial sodium channel; transient receptor potential vanilloid-1; electrophysiology SALT-TASTE DETECTION DEPENDS upon two salt-sensing transduction pathways that involve specialized membrane channels on the surface of fungiform taste bud cells in rats. One is the well-documented epithelial sodium channel (ENaC) that is selective for the sodium cation and can be blocked pharmacologically by amiloride. The other is not well understood in the rodent taste system, but has recently been hypothesized to be a variant of the nonspecific-cation channel of the transient receptor potential (TRP) family, TRP vanilloid-1 (TRPV1t) (Lyall et al. 2004), which is broadly receptive to several cations, sodium as well as potassium, calcium, and ammonium. These two salt-sensing pathways in fungiform taste bud cells communicate with two divergent afferent neuron groups in the chorda tympani (CT) nerve. Narrowly tuned NaCl-specialist neurons respond selectively to sodium (and lithium) salts and little, if at all, to other salts or other basic taste stimuli. ENaC antagonists attenuate NaCl responses of NaCl-specialist neurons, but not...

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To date, only one study has examined responses to monosodium glutamate (MSG) from gustatory neurons in the rat geniculate ganglion and none to free fatty acids. Accordingly, we recorded single-cell responses from geniculate ganglion gustatory neurons in anesthetized male rats to MSG and linoleic acid (LA), as well as to sucrose, NaCl, citric acid, and quinine hydrochloride. None of the 52 neurons responded to any LA concentration. In contrast, both narrowly tuned groups of gustatory neurons (sucrose specialists and NaCl specialists) responded to MSG, as did 2 of the broadly tuned groups (NaCl generalist(I) and acid generalists). NaCl-generalist(II) neurons responded only to the highest MSG concentration and only at low rates. No neuron type responded best to MSG; rather, responses to 0.1 M MSG were significantly less than those to NaCl for Na(+) -sensitive neurons and to sucrose for sucrose specialists. Interestingly, most Na(+) -sensitive neurons responded to 0.3 M MSG at levels comparable with those to 0.1 M NaCl, whereas sucrose specialists responded to 0.1 M MSG despite being unresponsive to NaCl. These results suggest that the stimulatory effect of MSG involves activation of sweet- or salt-sensitive receptors. We propose that glutamate underlies the MSG response of sucrose specialists, whereas Na(+) -sensitive neurons respond to the sodium cation. For the latter neuron groups, the large glutamate anion may reduce the driving force for sodium through epithelial channels on taste cell membranes. The observed concentration-dependent responses are consistent with this idea, as are cross-adaptation studies using 0.1 M concentrations of MSG and NaCl in subsets of these Na(+) -sensitive neurons.