Alterations of salt taste perception in the developing rat

Behavioral correlates of changing neurophysiological taste sensitivities during development were assessed with a conditioned taste aversion procedure. Young rats (age 25-30 days) avoided 0.1M monochloride salts and 1.0M sucrose reliably less than adults (age 90-105 days), but the two groups did not differ when the conditioned stimulus (CS) was 0.1M citric acid. Analyses of generalization gradients revealed that young rats were unable to discriminate among the tastes of NaCl, NH4Cl, and KCl, whereas adults readily made such discriminations. Both age groups had similar generalization gradients when the CS was 1.0M sucrose or 0.1M citric acid. These data indicate that quantitative and qualitative aspects of salt taste perception alter with age. Furthermore, the behavioral changes noted in the present study correspond closely with previous findings from developmental studies of neurophysiological taste responses.     

Lack of amiloride sensitivity in SHR and WKY glossopharyngeal taste responses to NaCl.

To explore possible functional strain differences in taste receptors located on the posterior tongue, we recorded electrophysiological taste responses from the glossopharyngeal nerve of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Multifiber responses to a concentration series (0.5 M to 2.0 M) of NaCl, KCl and NH4Cl were recorded before and after lingual application of the epithelial sodium transport blocker, amiloride. Responses to a concentration series (0.0025 M to 0.1 M) of quinine hydrochloride were also recorded. When expressed relative to the 0.5-M NH4Cl response, responses to the monochloride salts were equivalent between SHR and WKY. Surprisingly, NaCl responses were not suppressed by the sodium transport blocker, amiloride. This is in direct contrast to the dramatic suppression observed in the chorda tympani. Also, relative responses to quinine were greater in the glossopharyngeal nerve of SHR than WKY. These results indicate that taste receptors innervated by the glossopharyngeal nerve lack amiloride sensitivity and that posterior taste receptor function to monochloride salts is equivalent between SHR and WKY.     

Development of taste responses in the rat parabrachial nucleus

Extracellular responses from neurons in the parabrachial nuclei (PBN) were studied in rats 4 days old to adulthood during chemical stimulation of the tongue with monochloride salts, citric and hydrochloric acids, sucrose, sodium saccharin, and quinine hydrochloride. Multiunit taste responses were recorded in rats at 4-7 days of age and single-unit responses were recorded from 121 neurons in four other age groups of 14-20 days, 25-35 days, 50-60 days, and adults. PBN neurons in rats 4-7 days old consistently responded to 0.1 M solutions of NH4Cl and NaCl, to 0.5 M solutions of NH4Cl, NaCl, and KCl, and to 1.0 M sucrose, 0.1 M sodium saccharin, 0.1 M citric acid, and 0.1 N HCl. They often did not respond, however, to 0.1 M KCl and 0.01 M quinine hydrochloride. Single PBN neurons in rats 14 days old and older characteristically responded to all stimuli, which consisted of 0.1 and 0.5 M salts, acids, sucrose, sodium saccharin, and quinine hydrochloride. Thus no developmental differences occurred in the number of stimuli to which neurons responded after rats were 14 days old. With the exception of responses to hydrochloric acid, there were significant increases in response frequencies to all stimuli after 14 days of age. Average response frequencies to NH4Cl and citric acid increased after 20 days of age and those to NaCl, LiCl, KCl, sucrose, sodium saccharin, and quinine hydrochloride increased after 35 days of age. Average response frequencies for hydrochloric acid did not alter after 14 days of age. The proportion of single PBN neurons that responded maximally to specific monochloride salts did not change during development. Most single neurons in all age groups responded equally well to NH4Cl, NaCl, and LiCl. No PBN neuron responded maximally to KCl. Developmental differences in response frequencies of third-order gustatory neurons in the PBN generally reflect developmental response changes in first-order neurons of the chorda tympani nerve and second-order neurons of the solitary nucleus. However, unique developmental changes are evident in the PBN. Thus the ontogenetic changes that occur in PBN responses likely relate to modifications of lower-order peripheral and central nervous system afferents and peripheral receptor sensitivities.     

Development of taste responses in rat nucleus of solitary tract

Extracellular responses from neurons in the nucleus of the solitary tract (NST) were studied in rats aged 5 days to adulthood during chemical stimulation of the tongue with monochloride salts, citric and hydrochloric acids, sucrose, sodium saccharin, and quinine hydrochloride. Multiunit taste responses were recorded in rats at 5-7 days of age and single-unit responses were recorded from 111 neurons in four other age groups of 14-20 days, 25-35 days, 50-60 days, and adult. NST neurons in rats aged 5-7 days consistently responded to relatively high concentrations (0.5 M) of NH4Cl and KCl and to citric and hydrochloric acid. However, they often did not respond to 0.5 M NaCl or to 0.1 M NH4Cl. Single NST neurons in rats aged 14 days and older characteristically responded to all 0.1 and 0.5 M salts and to both acids. At least 75% of neurons also responded to sucrose and sodium saccharin, and 46% responded to all of these stimuli and quinine hydrochloride. After 14 days, no developmental changes occurred in the number of stimuli to which neurons responded. There were substantial developmental alterations in the response magnitudes to some chemical stimuli. Average response frequencies increased after 35 days of age for 0.1 and 0.5 M NaCl, LiCl, KCl, and for sucrose and sodium saccharin. Response frequencies for NH4Cl, citric and hydrochloric acid, and quinine hydrochloride, however, did not change throughout development. The proportion of single NST neurons that responded maximally to specific monochloride salts did not change during development. Most single neurons in all age groups responded equally well to NH4Cl, NaCl, and LiCl. No NST neuron responded maximally to KCl. There were also no developmental differences in response latencies in rats aged 14 days and older. Response frequencies of second-order NST neurons generally reflect changes in responses from the primary afferent, chorda tympani fibers, throughout development; however, the increases in salt response frequencies from NST neurons occur comparatively later in development. Furthermore, at all ages, the taste responses to monochloride salts include higher response frequencies and a general loss in response specificity in NST compared to chorda tympani neurons.(ABSTRACT TRUNCATED AT 400 WORDS)     

Neural representation of salts in the rat solitary nucleus: brain stem correlates of taste discrimination

One mechanism of salt taste transduction by gustatory receptor cells involves the influx of cations through epithelial sodium channels that can be blocked by oral application of amiloride. A second mechanism is less clearly defined but seems to depend on electroneutral diffusion of the salt through the tight junctions between receptor cells; this paracellular pathway is insensitive to amiloride. Because the first mechanism is more sensitive to sodium salts and the second to nonsodium salts, these peripheral events could underlie the ability of rats to discriminate sodium from nonsodium salts on the basis of taste. Behavioral experiments indicate that amiloride, at concentrations that are tasteless to rats, impairs a rat's ability to discriminate NaCl from KCl and may do so by making both salts taste like KCl. In the present study, we examined the neural representation of NaCl and KCl (0.05-0.2 M), and mixtures of these salts with amiloride (0, 3, and 30 microM), to explore the neural correlates of this behavioral result. NaCl and KCl were represented by distinct patterns of activity in the nucleus of the solitary tract. Amiloride, in a concentration-dependent manner, changed the pattern for NaCl to one more characteristic of KCl, primarily by reducing activity in neurons responding best to NaCl and sucrose. The effect of amiloride concentration on the response to 0.1 M NaCl in NaCl-best neurons was virtually identical to its effect on behavioral discrimination performance. Modeling the effects of blocking the amiloride-insensitive pathway also resulted in highly similar patterns of activity for NaCl and KCl. These results suggest that activity in both the amiloride-sensitive and -insensitive pathways is required for the behavioral discrimination between NaCl and KCl. In the context of published behavioral data, the present results suggest that amiloride-sensitive activity alone is not sufficient to impart a unique signal for the taste of sodium salts.     

Electrophysiological and behavioral studies on the taste of umami substances in the rat.

Electrophysiological and behavioral experiments were performed to reveal taste properties of "umami" substances such as monosodium glutamate (MSG) and disodium inosine monophosphate (IMP) in rats. To eliminate the taste effects of Na ions contained in these umami substances, we dissolved them in 0.01 mM amiloride, which is known to block sodium responses. In the electrophysiological study, taste responses of the whole chorda tympani nerve were recorded. The magnitude of responses to MSG (or IMP) at concentrations below 0.1 M (or 0.01 M) was less than 10% of that to 0.1 M NaCl. On the other hand, the mixtures of MSG and IMP showed responses 2-7 times larger than the arithmetric sum of the responses to each component of the mixtures. A new sweet taste inhibitor (Gymnema sylvestre extract) strongly suppressed neural responses to mixtures of MSG and IMP as well as sucrose, but only weakly or negligibly to individual solutions of these umami substances. In the behavioral study, the brief exposure two-bottle preference test and conditioned taste aversion paradigm were used. MSG was most preferred at 0.3 M (preference ratio = 57%), IMP, at 0.01 M (61%), and both were less preferred or rejected at higher concentrations. In contrast, mixtures of MSG and IMP were more preferred at a broad concentration range (e.g., 82% for 0.1 M MSG + 0.01 M IMP). Aversive conditioning to umami substances was generalized to sucrose, and vice versa, but not to 0.1 M NaCl, 0.01 M HCl, and 0.1 mM quinine hydrochloride.(ABSTRACT TRUNCATED AT 250 WORDS)     

Conditioned food aversion elicited by the temperature of drinking water as a conditioned stimulus in rats

It is known that taste can act as a conditioned stimulus (CS) for conditioned food aversion. In the present study, in order to examine whether or not the temperature of drinking water can be a CS, we conducted behavioral experiments in Wistar rats. The following results were obtained: (1) The rats subjected to aversive conditioning to 5 or 40 degrees C distilled water could learn to avoid these CSs, but they did not avoid any taste stimuli. (2) The rats subjected to aversive conditioning to 5 or 40 degrees C 0.1 M sucrose developed a generalized avoidance to sucrose at any temperature. (3) When rats familiarized to 25 degrees C 5 mM saccharin-Na (Sacc) were subjected to aversive conditioning to 5 or 40 degrees C Sacc, they avoided the respective CS, but they did not generalize it to any other stimuli even if having the same temperature as the CS. (4) The rats which had undergone transection of the taste nerves (chorda tympani and glossopharyngeal nerves) could acquire the conditioned response to the temperature of the CS. These results suggest that rats can be conditioned to temperature aversion and that the taste nerves are not needed in the formation of this conditioning.     

Peripheral taste responses in genetically hypertensive rats

In two-bottle preference-aversion tests, the spontaneously hypertensive rat (SHR) tolerates higher concentrations of NaCl than the normotensive Wistar-Kyoto (WKY). In contrast, the inbred Dahl salt-sensitive (S/JR) and inbred Dahl salt-resistant (R/JR) rat show similar preferences for NaCl. In order to determine if taste receptor function was also altered between the hypertensive rat and its normotensive control, we recorded electrophysiological taste responses from the chorda tympani (CT) nerve in SHR, WKY, S/JR and R/JR rats. Responses to a concentration series (0.05 M to 0.5 M) of NaCl, NaAcetate, KCl, NH4Cl and CaCl2 were recorded before and after lingual application of amiloride hydrochloride, an epithelial sodium transport blocker. When expressed relative to the 0.5 M NH4Cl response, responses to the majority of stimuli were equivalent between the SHR and WKY. By comparison, relative responses to NaCl were greater in the R/JR than S/JR; however, the magnitude of amiloride suppression was equivalent between these two strains. Relative responses to the majority of the remaining salts did not differ between the S/JR and R/JR. These results suggest that taste receptor function may be equivalent between the hypertensive rat and its normotensive control.     

Central gustatory lesions and learned taste aversions: unconditioned stimuli

The efficacy of two different unconditioned stimuli (US) in producing conditioned taste aversion (CTA) was tested in rats after bilateral ibotenic acid (IBO) lesions of the gustatory nucleus of thalamus (TTAx) and the medial and lateral parabrachial nuclei (mPBNx, lPBNx). An initial study determined an equivalent dose for the two USs, LiCl and cyclophosphamide (CY), using non-lesioned rats. Subsequently, using a separate set of lesioned animals and their sham controls (SHAM), injections of CY were paired 3 times with one of two taste stimuli (CSs), 0.1 M NaCl for half the rats in each group, 0.2 M sucrose for the other half. After these conditioning trials, the CS was presented twice more without the US, first in a 1-bottle test, then in a 2-bottle choice with water. The acquisition and test trials had 2 intervening water-only days to assure complete rehydration. Two weeks later, the same rats were tested again for acquisition of a CTA using LiCl as the US and the opposite CS as that used during the CY trials. The SHAM and TTAx groups learned to avoid consuming the taste associated with either CY or LiCl treatment. The two PBNx groups failed to learn an aversion regardless of the US.     

Estrogen increases the taste threshold for sucrose in rats

Anecdotal and empirical evidence suggests that females' preferences for sweet foods are affected by hormonal fluctuations across the reproductive cycle. In rats, the preference for sweet foods may involve estrogen-mediated changes in response to the taste of sweets. Our recent work showed that ovariectomized female rats lick less to dilute sucrose solutions when given estrogen than when given the oil vehicle. These findings suggest that estrogen decreases the preference for less concentrated sucrose solutions; however, an alternative explanation is that estrogen interferes with the ability to detect dilute sucrose solutions. To distinguish between these possibilities, we conditioned a taste aversion to 0.2 M sucrose in ovariectomized rats by pairing it with injection of LiCl and then examined the generalization of that taste aversion to 0.075 and 0.025 M sucrose solutions during estrogen or oil treatment. Oil-treated rats generalized the LiCl-induced aversion conditioned to 0.2 M sucrose to both 0.075 and 0.025 M sucrose. Estrogen-treated rats generalized the LiCl-induced taste aversion to 0.075 M sucrose but not to 0.025 M sucrose. Moreover, two weeks later, when estrogen had cleared the system, both groups generalized the aversion to both 0.075 and 0.025 M sucrose. These results show that estrogen affects the ability to discriminate dilute sucrose from water and suggest that estrogen may have short-term effects on the detection threshold for sucrose taste in rats.     

Centrifugal inputs modulate taste aversion learning associated parabrachial neuronal activities

Our previous studies have demonstrated that gustatory neurons in the parabrachial nucleus (PBN) show altered responses after the acquisition of conditioned taste aversion (CTA) to NaCl. The present study was conducted 1) to examine centrifugal influences on the altered gustatory activity of CTA-trained rats, and 2) to evaluate the role of amiloride-sensitive (ASN) and -insensitive NaCl (AIN) best units in coding the taste of NaCl. Animals were separated into 2 groups: a CTA group that had acquired taste aversion to 0.1 M NaCl and a control group that underwent pseudoconditioning before the recording experiment. Single-neuron activity, in 2 separate series of experiments, was extracellularly recorded in anesthetized rats. In the stimulation studies, the effects of electrical stimulation of the gustatory cortex (GC) or the central nucleus of amygdala (CeA) were examined on firing of PBN taste units. CeA stimulation produced excitatory effect in significantly more neurons in the CTA group (n = 8) than in the control group (n = 1). Furthermore, ASN-best units in the CTA group showed larger responses to NaCl than similar units in the control group. In the decerebration experiment, there was no statistical difference among the taste responses between the 2 groups in any best-stimulus category. These results suggest that CTA conditioning uses an effective central amygdaloid input to modulate activity of gustatory neurons in the PBN. Data also substantiate that amiloride-sensitive components of NaCl-best neurons play a critical role in the recognition of distinctive taste of NaCl.     

A novel pharmacological probe links the amiloride-insensitive NaCl, KCl, and NH(4)Cl chorda tympani taste responses.

Chorda tympani taste nerve responses to NaCl can be dissected pharmacologically into amiloride-sensitive and -insensitive components. It is now established that the amiloride-sensitive, epithelial sodium channel acts as a sodium-specific ion detector in taste receptor cells (TRCs). Much less is known regarding the cellular origin of the amiloride-insensitive component, but its anion dependence indicates an important role for paracellular shunts in the determination of its magnitude. However, this has not precluded the possibility that undetected apical membrane ion pathways in TRCs may also contribute to its origin. Progress toward making such a determination has suffered from lack of a pharmacological probe for an apical amiloride-insensitive taste pathway. We present data here showing that, depending on the concentration used, cetylpyridinium chloride (CPC) can either enhance or inhibit the amiloride-insensitive response to NaCl. The CPC concentration giving maximal enhancement was 250 microM. At 2 mM, CPC inhibited the entire amiloride-insensitive part of the NaCl response. The NaCl response is, therefore, composed entirely of amiloride- and CPC-sensitive components. The magnitude of the maximally enhanced CPC-sensitive component varied with the NaCl concentration and was half-maximal at [NaCl] = 62 +/- 11 (SE) mM. This was significantly less than the corresponding parameter for the amiloride-sensitive component (268 +/- 71 mM). CPC had similar effects on KCl and NH(4)Cl responses except that in these cases, after inhibition with 2 mM CPC, a significant CPC-insensitive response remained. CPC (2 mM) inhibited intracellular acidification of TRCs due to apically presented NH(4)Cl, suggesting that CPC acts on an apical membrane nonselective cation pathway.     

The suppressive effects of LiCl, sucrose, and drugs of abuse are modulated by sucrose concentration in food-deprived rats.

Suppression of intake of a gustatory conditioned stimulus (CS) occurs when paired with either an aversive or an appetitive unconditioned stimulus (US). Toxic substances, such as lithium chloride (LiCl), induce conditioned taste aversions while rewarding stimuli, such as high a concentration of sucrose, reduce intake through a comparison process referred to as anticipatory contrast. Drugs of abuse also suppress CS intake, but it is not known whether they do so via their rewarding or aversive properties. Using 0.1, 0.3, or 0.5 M sucrose solutions as the gustatory CS, we compared the suppressive effects of LiCl (5.29 mg/kg), morphine (15 mg/kg), cocaine (10 mg/kg), and a 1.0-M sucrose solution in rats that were food deprived. The doses of the three drugs have been equated in terms of their suppressive effects in water-deprived and free-feeding rats. The results showed that in food-deprived rats the sucrose US failed to suppress intake of any of the sucrose CSs, the drugs of abuse failed to suppress intake of the 0.3 and 0.5-M concentration of sucrose, and LiCl failed to suppress intake of the 0.5-M sucrose solution. When taken together, these findings reveal that the suppressive effects of all USs (aversive, appetitive, and drugs of abuse) can be offset by the use of a caloric CS when evaluated in food-deprived rats.     

Inhibition of taste responses to Na+ salts by epithelial Na+ channel blockers in gerbil

The Na+ transport inhibitor amiloride blocks taste responses to NaCl by 60-70%. The purpose of the present study was to determine if greater inhibition could be achieved with three potent amiloride analogs that are specific for the epithelial Na+ channel: phenamil, 2',4'-dimethylbenzamil, and 3',4'-dichlorobenzamil. Application of phenamil (100 microM) to the anterior tongue blocked integrated responses to NaCl from the chorda tympani nerve by 98.04%, but had no significant effect on sucrose or NH4Cl. This finding suggests that the epithelial Na+ channel alone transduces the taste of NaCl in gerbil. The residual 30-40% of the response that is not blocked by amiloride can simply be explained by the fact that amiloride is less potent than phenamil. On average, 100 microM phenamil blocked responses to Na+ salts with a variety of anions by 94.2%; 100 microM 2',4'-dimethylbenzamil, by 89.83%; and 100 microM 3',4'-dichlorobenzamil, by 72.56%. Small residual responses to salts of glutamate and phosphate were not eliminated by the amiloride analogs; this suggests that other transduction mechanisms may account for a small portion of taste responses for these salts in the gerbil.     

Amiloride increases sodium chloride taste detection threshold in rats

The epithelial sodium-channel blocker amiloride has been shown to inhibit sodium responses in the 7th cranial nerve of the rat. In the signal detection task used in this study, amiloride (100 microM) treatment raised the NaCl threshold by approximately 1 log10 unit. The inhibition constant for amiloride was 1 microM at 0.013 M NaCl. Because the NaCl intake of adult rats has been shown to be related to the level of dietary NaCl exposure early in development, rats were exposed by way of maternal diet to 1 of 3 diets (0.1% NaCl, n = 8; 1.0% NaCl, n = 8; 3.0% NaCl, n = 9) from conception through weaning, to determine whether this treatment affects taste sensitivity. At Postnatal Day 30, rats were placed on 1.0% NaCl chow. This treatment did not affect NaCl detection or amiloride sensitivity in adulthood. The amiloride-induced shifts in NaCl sensitivity functions imply that the transcellular sodium transduction pathway is necessary for normal NaCl detection in the rat.     

Conditioned taste aversions: generalization to taste mixtures

Rats were trained to take their daily water ration within a 30-min session, during which the number of licks per 10-sec presentation of a drinking tube could be recorded. During one of these sessions, one of three stimuli (sucrose, NaCl or HCl) was presented, followed by the administration of cyclophosphamide to produce a conditioned taste aversion. When tested with mixtures of the conditioned stimulus (CS) with the other two stimuli and also with quinine hydrochloride, the animals avoided mixtures containing the CS in proportion to its concentration in the mixture. Although the natural preferences and aversions for these stimuli interacted somewhat with the learned taste aversions, rats responded to the presence of a CS in a mixture and did not generalize to other stimuli not containing the CS. Thus, the generalization of conditioned taste aversions provides a good measure of the behavioral similarities among gustatory stimuli.     

Taste reactivity as a dependent measure of the rapid formation of conditioned taste aversion: a tool for the neural analysis of taste-visceral associations

Several explanations may account for deficits in the ability of animals to form taste aversions following neural manipulations. These encompass impairments in conditioned stimulus (CS) and unconditioned stimulus (US) processing, conditioned response (CR) measurement, and expression, memory, and taste-visceral integration. A behavioral procedure that aids in the distinction between some of these possibilities is presented. In Experiment 1, 10 rats received seven intraoral (IO) infusions of sucrose (30 s, 0.55 ml) spaced every 5 min starting immediately after the injection of 3.0 mEq/kg of lithium chloride (LiCl). Control rats (n = 12) were treated identically except that they were injected with sodium chloride (NaCl). Oromotor and somatic taste reactivity behaviors were videotaped and analyzed. Lithium-injected rats systematically decreased their ingestive taste reactivity behavior over time, whereas aversive behavior increased. Control rats maintained high and stable levels of ingestive responding and demonstrated virtually no aversive behavior over the 30-min period following sodium injection. Rats were tested several days later for the presence of a conditioned taste aversion (CTA). Rats previously injected with lithium during sucrose infusions demonstrated significantly more aversive behavior than the control group, which demonstrated none. There were no differences in the level of ingestive behavior displayed by the two groups on the CTA test. Experiment 3 revealed that when similarly treated rats were tested for a CTA while in a lithium-induced state, a difference in the ingestive behavior between the two groups was observed. In Experiment 2, naive rats were injected with either NaCl or LiCl but did not receive their first sucrose infusion until 20 min later. These rats also received sucrose infusions at 25 and 30 min postinjection. There were no differences in the taste reactivity behavior displayed by lithium- or sodium-injected rats during any of the sucrose infusions. Collectively, these findings indicate that rats dramatically change their oromotor responses to sucrose during the period following LiCl administration, provided that the infusions start immediately after injection. Furthermore, this time-related behavioral change is predominantly attributable to associative processes. This paradigm can be useful in distinguishing between neural manipulations that affect the establishment of taste-visceral associations from others that affect the animal's ability to retain such associations over the commonly employed 24-hr conditioning-test interval.     

Postconditioning recovery from the latent inhibition effect in conditioned taste aversion

Two experiments were conducted examining the effects of flavor (CS) preexposure on the retention of conditioned taste aversion. In Experiment 1, rats received preexposure to sucrose solution followed by a sucrose-illness pairing. The expected “latent inhibition” effect was obtained when testing occurred after a two-day but not an eleven-day training-to-test interval. Experiment 2 extended these results by employing five- and twenty-one-day training-to-test interval parameters and provided evidence that the stronger taste aversion displayed by preexposed subjects following long retention intervals is not attributable to differences in training consumption of sucrose solution. This posttraining increase in conditioned taste aversion (CTA) suggests that preexposure blocks expression of memory.     

Recall of a previously acquired conditioned taste aversion in rats following lesions of the area postrema

A conditioned taste aversion was produced by pairing a novel sucrose solution with either 3 mEq lithium chloride or with 100 rad gamma radiation in rats with the area postrema intact. Lesions of the area postrema were then made in half of the rats exposed to each treatment and in rats that were not treated with the unconditioned stimulus. When tested for a conditioned taste aversion, all treated rats showed a significant aversion to the sucrose solution compared to the untreated control rats. There were no significant differences between rats with area postrema lesions and those with the area postrema intact, indicating that the lesions had no effect on the recall of the previously acquired aversion. The results are interpreted as being consistent with the hypothesis that the role of the area postrema in taste aversion learning is to monitor blood and cerebrospinal fluid for potential toxins and to transmit that information to the central nervous system.     

Gustatory neuron types in rat geniculate ganglion

We used extracellular single-cell recording procedures to characterize the chemical and thermal sensitivity of the rat geniculate ganglion to lingual stimulation, and to examine the effects of specific ion transport antagonists on salt transduction mechanisms. Hierarchical cluster analysis of the responses from 73 single neurons to 3 salts (0.075 and 0.3 M NaCl, KCl, and NH(4) Cl), 0.5 M sucrose, 0.01 M HCl, and 0.02 M quinine HCl (QHCl) indicated 3 main groups that responded best to either sucrose, HCl, or NaCl. Eight narrowly tuned neurons were deemed sucrose-specialists and 33 broadly tuned neurons as HCl-generalists. The NaCl group contained three identifiable subclusters: 18 NaCl-specialists, 11 NaCl-generalists, and 3 QHCl-generalists. Sucrose- and NaCl-specialists responded specifically to sucrose and NaCl, respectively. All generalist neurons responded to salt, acid, and alkaloid stimuli to varying degree and order depending on neuron type. Response order was NaCl > HCl = QHCl > sucrose in NaCl-generalists, HCl > NaCl > QHCl > sucrose in HCl-generalists, and QHCl = NaCl = HCl > sucrose in QHCl-generalists. NaCl-specialists responded robustly to low and high NaCl concentrations, but weakly, if at all, to high KCl and NH(4) Cl concentrations after prolonged stimulation. HCl-generalist neurons responded to all three salts, but at twice the rate to NH(4) Cl than to NaCl and KCl. NaCl- and QHCl-generalists responded equally to the three salts. Amiloride and 5-(N,N-dimethyl)-amiloride (DMA), antagonists of Na(+) channels and Na(+)/H(+) exchangers, respectively, inhibited the responses to 0.075 M NaCl only in NaCl-specialist neurons. The K(+) channel antagonist, 4-aminopyridine (4-AP), was without a suppressive effect on salt responses, but, when applied alone in solution, it evoked a response in many HCl-generalists and one QHCl-generalist neuron so tested. Of the 39 neurons tested for their sensitivity to temperature, 23 responded to cooling and chemical stimulation, and 20 of these neurons were HCl-generalists. Moreover, the responses to the four standard stimuli were reduced progressively at lower temperatures in HCl- and QHCl-generalist neurons, but not in NaCl-specialists. Thus sodium channels and Na(+)/H(+) exchangers appear to be expressed exclusively on the membranes of receptor cells that synapse with NaCl-specialist neurons. In addition, cooling sensitivity and taste-temperature interactions appear to be prominent features of broadly tuned neuron groups, particularly HCl-generalists. Taken all together, it appears that lingual taste cells make specific connections with afferent fibers that allow gustatory stimuli to be parceled into different input pathways. In general, these neurons are organized physiologically into specialist and generalist types. The sucrose- and NaCl-specialists alone can provide sufficient information to distinguish sucrose and NaCl from other stimuli, respectively.