Sapid Stimuli Research Articles

Taste Responses in the Nucleus of the Solitary Tract of Awake Obese Rats Are Blunted Compared With Those in Lean Rats.

Taste perception changes with obesity but the underlying neural changes remain poorly understood. To address this issue, we recorded taste responses from single cells in the nucleus tractus solitarius (NTS, the first synapse in the central gustatory circuit) in awake, diet-induced obese [(DIO; ≥ 8 weeks on a high-energy diet (45%fat, 17% sugar; HED)], and lean rats. Rats were implanted with a bundle of microelectrodes in the NTS and allowed to recover. Water-deprived rats were allowed to freely lick various tastants in an experimental chamber. Taste stimuli included an array of sapid stimuli dissolved in artificial saliva (AS). Each taste trial consisted of five consecutive licks followed by five AS licks presented on a VR5 schedule. Results showed that taste responses (n = 49 for DIO; n = 74 for lean rats) in NTS cells in DIO rats were smaller in magnitude, shorter in duration, and longer in latency that those in lean rats. However, there were proportionately more taste-responsive cells in DIO than in lean rats. Lick coherence in DIO rats was significantly lower than in lean rats, both in taste-responsive, and lick-related cells (n = 172 in lean; n = 65 in DIO). Analyses of temporal coding showed that taste cells in DIO rats conveyed less information about taste quality than cells in lean rats. Collectively, results suggest that a HED produces blunted, but more prevalent, responses to taste in the NTS, and a weakened association of taste responses with ingestive behavior. These neural adaptations may represent both negative effects and compensatory mechanisms of a HED that may underlie deficits in taste-related behavior associated with obesity.

La cuestión de las sensaciones gustativas básicas

Background : There is interest in discovering more about the possible influence in taste perception and its effect in dietary selection and food behaviors. Objective : Explore the factors that alter perceptions of taste and their relationship with food consumption. Materials and methods: A literature review was performed using scientific databases: Science Direct, Medline y Pubmed on the subject of taste, regardless of dominant flavors. Results : Progress has been made on the physiological basis of the basic tastes: sweet, salty, sour, bitter and umami. It has recently been proposed to add a “fatty” taste but as of now no consensus exists. Taste and food selection depend on genetic factors, first experiences with sapid stimuli, even before birth, as well as cultural, social, individual and other factors related to food. An association between consumption of high-calorie foods and taste sensitivity has not been demonstrated, nor taste sensitivity with obesity. Conclusion : The effect of taste perception on food consumption and any relation with obesity continues to be controversial. It is recommended to educate from a young age on taste perception, with the goal of acquiring healthy food habits.

The Representation of Taste Quality in the Mammalian Nervous System

The process by which the mammalian nervous system represents the features of a sapid stimulus that lead to a perception of taste quality has long been controversial. The labeled-line (sparse coding) view differs from the across-neuron pattern (ensemble) counterpoint in proposing that activity in a given class of neurons is necessary and sufficient to generate a specific taste perception. This article critically reviews molecular, electro-physiological, and behavioral findings that bear on the issue. In the peripheral gustatory system, the authors conclude that most qualities appear to be signaled by labeled lines; however, elements of both types of coding characterize signaling of sodium salts. Given the heterogeneity of neuronal tuning functions in the brain, the central coding mechanism is less clear. Both sparse coding and neuronal ensemble models remain viable possibilities. Furthermore, temporal patterns of discharge could contribute additional information. Ultimately, until specific classes of neurons can be selectively manipulated and perceptual consequences assessed, it will be difficult to go beyond mere correlation and conclusively discern the validity of these coding models.

Altered taste sensitivity in obese, prediabetic OLETF rats lacking CCK-1 receptors

Otsuka Long-Evans Tokushima fatty (OLETF) rats lack the CCK-1 receptor, are hyperphagic, progressively become obese, and develop type-2 diabetes. We recently demonstrated an increased preference for both real and sham feeding of sucrose in this strain, suggesting altered orosensory sensitivity. To investigate taste functions, we used an automated gustometer with 10-s access to different concentrations of various sapid stimuli. Tests were repeated at 10 and 18 wk of age to assess the early and advanced stages of prediabetes, respectively. Compared with age-matched, nonmutant controls, the OLETF rats showed higher avidity for sucrose at both ages. This difference increased as a function of age and tastant concentration. An exaggerated response also occurred for saccharin, alanine, and fructose, but not for Polycose. Similarly, OLETF rats consumed monosodium-glutamate more at the lower concentrations compared with controls, an effect that age also accentuated. In contrast, there was no statistical strain or age differences in responses to NaCl, MgCl2, citric acid, quinine-HCl, and the trigeminal stimulus capsaicin. These findings demonstrate that compared with controls, OLETF rats differ in their gustatory functions with an overall augmented sensitivity for sweet that progresses during prediabetes. This effect explains their overconsumption of sweet solutions and may contribute to the overall hyperphagia and obesity in this strain.

Intracranial renin alters gustatory neural responses in the nucleus of the solitary tract of rats.

Activation of the renin-angiotensin system in the brain is considered important in the arousal and expression of sodium appetite. To clarify the effects of directly activating this hormonal cascade, taste neurons in the nucleus of the solitary tract of rats were tested with a battery of sapid stimuli after intracerebroventricular injection of renin or its vehicle. The rats were chronically prepared but lightly anesthetized during the recording procedure. Eighty-five taste neurons were tested: 46 after renin injections and 39 after vehicle. Neural activity was counted for 5.0-s periods without stimulation (spontaneous) and during stimulation with water and sapid chemicals. The averaged responses to each of the standard stimuli (0.1 M NaCl, 0.3 M sucrose, 0.01 M citric acid, and 0.01 M quinine hydrochloride) did not differ significantly between the two conditions. When the rats were tested with a concentration range of NaCl, however, after renin the average responses to the hypertonic 0.3 and 1.0 M stimuli were reduced to 74 and 70%, respectively, compared with those after vehicle injections. A similar tendency was evident for the subsample of neurons that responded best to NaCl, but the effect was smaller. These data are consistent with, but not as dramatic as, those reported after dietary-induced sodium appetite.

Responses to Taste Stimulation in the Ventroposteromedial Nucleus of the Thalamus in Rats

Extracellular action potentials were recorded from 73 neurons in the parvicellular division of the ventroposteromedial (VPMpc) nucleus of the thalamus of anesthetized Wistar rats during gustatory, thermal, and tactile stimulation of the whole oral cavity. The stimulus array consisted of 16 room-temperature (23 degrees C) sapid stimuli, distilled water at three temperatures (0, 23, and 37 degrees C), and 0.1 M NaCl at three temperatures (0, 23, and 37 degrees C). Among all 151 neurons isolated in VPMpc, 9% responded exclusively to taste, 33% to taste and temperature, none to taste and touch, but 6% to all three modalities. Discharge rates evoked by the basic tastants were 13.8 +/- 1.6 (SD) spikes/s for 0.1 M NaCl, 9.3 +/- 1.4 spikes/s for 0.01 M HCl, 5.1 +/- 0.9 spikes/s for 0.5 M sucrose, and 4.3 +/- 0.6 spikes/s for 0.01 M quinine HCl. Water evoked mean responses at 0, 23, and 37 degrees C of 9.9 +/- 1.5, 0.6 +/- 0.4, and 1.3 +/- 0.9 spikes/s, respectively. The mean firing rate evoked by 37 and 0 degrees C NaCl was 15.0 +/- 2.4 and 17.0 +/- 2.8 spikes/s, respectively. The exponent of the NaCl concentration-response power function was 0.39. Thalamic taste cells were broadly tuned. The mean breadth-of-tuning coefficient for these 73 gustatory cells was 0.79 +/- 0.02. Two cells responded predominantly with inhibition, which accounted for the majority of inhibitory responses. The taste neurons were statistically divisible into three groups: sodium-oriented (n = 40), acid-oriented (n = 12), and sugar-oriented (n = 17). Four additional bitter-oriented neurons were not closely enough related to be defined as a group and were considered outliers. The sodium-oriented group could be divided into three statistically distinct subgroups, differing in the specificity of their responses to NaCl. With respect to polymodal sensitivity, spontaneous rate, evoked response rates, signal-to-noise ratio, proportions of cells responding best to basic tastants, taste neuron groups, taste spaces, and temporal responses, VPMpc neurons have characteristics that are intermediate between those of parabrachial and cortical gustatory neurons.

Neural Correlates of Tasting Concentrated Quinine and Sugar Solutions

Behavioral, ethological, and electrophysiological evidence suggests that the highly unpleasant, bitter taste of a concentrated quinine hydrochloride (QHCL) should activate the human amygdala. In the present study, healthy subjects tasted 0.02 M QHCL or water while regional cerebral blood flow (rCBF) was assayed with H(2)(15)O PET. Subjects were also studied while tasting a pleasant sucrose solution and resting with eyes closed (ECR). Tasting QHCL significantly increased rCBF within the left amygdala relative to control conditions of tasting water and ECR. Sucrose and water caused small to moderate rCBF increases in the amygdala relative to ECR, but sucrose did not significantly increase activity within either amygdalae relative to water. In the frontal lobe, QHCL and sucrose both activated the right posterior orbitofrontal cortex (OFC) relative to water, but portions of the anterior OFC and inferior frontal pole showed valence specific responses to QHCL. These data indicate that the left amygdala responds robustly to QHCL and more moderately to nonaversive sapid stimuli, both pleasant and unpleasant gustatory stimuli activate the right posterior OFC, and the left inferior frontal pole/anterior OFC demonstrates valence-specific responses to aversive gustatory stimuli.

Pontine gustatory activity is altered by electrical stimulation in the central nucleus of the amygdala.

Visceral signals and experience modulate the responses of brain stem neurons to gustatory stimuli. Both behavioral and anatomical evidence suggests that this modulation may involve descending input from the forebrain. The present study investigates the centrifugal control of gustatory neural activity in the parabrachial nucleus (PBN). Extracellular responses were recorded from 51 single PBN neurons during application of sucrose, NaCl, NaCl mixed with amiloride, citric acid, and QHCl with or without concurrent electrical stimulation in the ipsilateral central nucleus of the amygdala (CeA). Based on the sapid stimulus that evoked the greatest discharge, 3 neurons were classified as sucrose-best, 32 as NaCl-best, and 16 as citric acid-best. In most of the neurons sampled, response rates to an effective stimulus were either inhibited or unchanged during electrical stimulation of the CeA. Stimulation in the CeA was without effect in two sucrose-best neurons, nine NaCl-best neurons, and one citric acid-best neuron. Suppression was evident in 1 sucrose-best neuron, 18 NaCl-best neurons, and 15 citric acid-best neurons. In NaCl-best neurons inhibited by CeA stimulation, the magnitude of the effect was similar for spontaneous activity and responses to the five taste stimuli. Nonetheless, the inhibitory modulation of gustatory sensitivity increased the relative effectiveness of NaCl resulting in narrower chemical selectivity. For citric acid-best neurons, the magnitude of inhibition produced by CeA activation increased with an increase in stimulus effectiveness. The responses to citric acid were inhibited significantly more than the responses to all other stimuli with the exception of NaCl mixed with amiloride. The overall effect was to change these CA-best neurons to CA/NaCl-best neurons. In a smaller subset of NaCl-best neurons (n = 5), CeA stimulation augmented the responsiveness to NaCl but was without effect on the other stimuli or on baseline activity. It appears that electrical stimulation in the CeA modulates response intensity, as well as the type of gustatory information that is transmitted in a subset of NaCl-best neurons. These findings provide an additional link between the amygdala and the PBN in the control of NaCl intake, modulating the response and the chemical selectivity of an amiloride-sensitive Na+ detecting input pathway.

Rat amygdalar neuronal responses during licking of sapid stimuli and discrimination of various conditioned sensory stimuli

The subdivisions of the sacral intermediolateral nucleus (IML) of the cat have been studied by using a double-labeling technique of retrograde Fluoro-gold (FG) and wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) tracing. The parasympathetic preganglionic neurons (PGNs) that were labeled by the FG injected into the pelvic nerve formed a ‘V’-shaped column known as the sacral parasympathetic nucleus (SPN) in the sacral IML. The neurons that were labeled by the WGA-HRP applied to the lateral parabrachial nucleus (PBL) formed an elongated spindle-shaped column extending throughout the IML of the sacral segments. We designated it by the name of sacral visceral sensory nucleus (SVSN). These findings indicate that the sacral IML of the cat contain two distinct subdivisions, SPN and SVSN.

Gustatory and multimodal neuronal responses in the amygdala during licking and discrimination of sensory stimuli in awake rats.

The amygdala (AM) receives information from various sensory modalities via the neocortex and directly from the thalamus and brain stem and plays an important role in ingestive behaviors. In the present study, neuronal activity was recorded in the AM and amygdalostriatal transition area of rats during discrimination of conditioned sensory stimuli and ingestion of sapid solutions. Of the 420 responsive neurons, 227 responded exclusively to one sensory modality, 120 responded to two or more modalities, and the remaining 73 could not be classified. Among the responsive neurons, 108 responded to oral-sensory stimulation (oral-sensory neurons). In detailed analyses of 84 of these oral-sensory neurons, 24 were classified as taste responsive and were located mainly in the central nucleus of the AM. The other 60 oral-sensory neurons were classified as nontaste oral-sensory neurons and were distributed widely throughout the AM. Both the taste and nontaste oral-sensory neurons also responded to other sensory stimuli. Of the 24 taste neurons, 21 were tested at least with four standard taste solutions. On the basis of the magnitudes of their responses to these sapid stimuli, the taste neurons were classified as follows: seven sucrose-best, four NaCl-best, three citric acid-best, and six quinine HCl-best. The remaining cell responded significantly only to lysine HCl and monosodium glutamate. Multivariate analyses of these 21 taste neurons suggested that, in the AM, taste quality was processed based on palatability. Taken with previous lesion studies, the present results suggest that the AM plays a role in the evaluation of taste palatability and in the association of taste stimuli with other sensory stimuli.

Somatostatin administration alters taste preferences in the rat

The effects of long-term and relatively constant concentrations of somatostatin (SRIF) were tested in rats to investigate its influence on taste preferences, fluid intake, and taste bud topography of the tongue. In SRIF-treated rats, intake of 3 × 10 −2 M NaCl and 6 × 10 −2 M sucrose solution decreased, whereas that of 3 × 10 −5 M quinine-HCl and 10 −3 M HCl (pH = 3) solutions increased significantly; distilled water intake and total fluid consumption remained almost unchanged. The light/dark cycle of consumption of NaCl solution was modified in a dose-dependent manner, but that of dwater, total fluids, and other solutions was not. Histologic exam by light microscopy showed that taste bud distribution on the tongue appeared to be altered, but the results only approached statistical significance. Given that it is possible to remove virtually all taste buds in the oral cavity and have only modest effects on preferences and aversion, it seems very unlikely that the small changes in taste bud distribution are related to the intake of sapid solutions. Since SRIF treatment influenced all sapid stimuli, it seems more likely that the changes are based on a blunted responsiveness in the gustatory system as a whole.

Parabrachial neural coding of taste stimuli in awake rats.

Parabrachial neural coding of taste stimuli in awake rats. J. Neurophysiol. 78: 2254-2268, 1997. In awake, behaving rats, the activity of 74 single neurons in the pontine parabrachial nucleus (PBN) was recorded in response to sapid stimulation by 15 chemicals. Of these, 44 taste cells were tested with all 15 stimuli. Based on their responsiveness to 4 standard stimuli, these neurons were categorized as follows: 23 NaCl-best, 15 sucrose-best, 5 citric acid-best, and 1 quinine HCl-best. Several forms of multivariate analyses indicated that the taste responses matched both the behavioral responses to and, less well, the chemical structure of, the sapid stimuli. A hierarchical cluster analysis of the neurons substantially confirmed the best-stimulus categorization, but separated the NaCl-best cells into those that responded more to Na+-containing salts and those that responded more to Cl--containing salts. The cells that responded best to the Na+ moiety actually were somewhat more correlated with the sucrose-best cells than with those that responded to the Cl--containing stimuli. Citric acid-best neurons and the lone quinine-best unit formed a single cluster of neurons that responded well to acids, as well as to NH4Cl and, to a lesser extent, NaNO3. A factor analysis of the neuronal response profiles revealed that three factors accounted for 78.8% of the variance in the sample. Similar analyses of the stimuli suggested that PBN neurons respond to four or five sets of stimuli related by their chemical makeup or by human psychophysical reports. The capacity of rats to make these discriminations has been documented by other behavioral studies in which rodents generalize across sapid chemicals within each of 5 stimulus categories. Furthermore, a simulation analysis of the neural data replicated behavioral results that used amiloride, a Na+ channel blocker, in which rats generalized NaCl to non-Na+, Cl- salts. Thus, using a variety of analyses, in awake rats, the activity of PBN taste neurons tracks their behavioral responses to a variety of chemical stimuli.

Electrophysiological evidence for two transduction pathways within a bitter-sensitive taste receptor.

Among the sapid stimuli, those that elicit bitter taste are the most abundant and structurally diverse. To accommodate this diversity, animals are thought to use multiple bitter transduction pathways. We examined the role of individual taste receptor cells (TRCs) in this transduction process by focusing on one of the taste organs, or chemosensilla, of a caterpillar (Manduca sexta). This chemosensillum (the lateral styloconicum) contains four functionally distinct TRCs: the salt, sugar, inositol, and deterrent TRCs, which are known to respond strongly to, in respective order, salts, sugars, inositol, and compounds humans describe as bitter. Using an extracellular recording technique, we tested three hypotheses for how a structurally diverse array of bitter compounds (salicin, caffeine, and aristolochic acid) could excite the same chemosensillum: several TRCs within the lateral styloconica respond to the bitter compounds; only the deterrent TRC responds to the bitter compounds, through a single transduction pathway; and only the deterrent TRC responds to the bitter compounds, but through multiple transduction pathways. To discriminate among these hypotheses, we tested five predictions. The first addressed how many TRCs within the lateral styloconica responded to the bitter compounds. Subsequent predictions were based on the results of the test of the first prediction and assumed that only the deterrent TRC responded to these compounds. These latter predictions addressed whether the bitter compounds acted through one or multiple transduction pathways. We obtained evidence consistent with the third hypothesis: only the deterrent TRC responded to the bitter compounds; the temporal patterns of firing and concentration-response curves elicited by caffeine and salicin were similar to each other, but different from those elicited by aristolochic acid; the patterns of sensory adaptation and disadaptation elicited by caffeine and salicin were similar to each another, but different from those elicited by aristolochic acid; reciprocal cross-adaptation occurred between caffeine and salicin, but not between aristolochic acid and caffeine or aristolochic acid and salicin; and the responsiveness of individual deterrent TRCs to caffeine and salicin correlated significantly, whereas that to aristolochic acid and caffeine or aristolochic acid and salicin did not. Taken together, these results indicate that the deterrent TRC contains at least two excitatory transduction pathways: one responds to caffeine and salicin and the other to aristolochic acid. To our knowledge, this is the first direct support for the existence of two bitter transduction pathways within a single TRC.

Single taste stimuli elicit either increases or decreases in intracellular calcium in isolated catfish taste cells.

Taste cells are specialized epithelial cells that respond to stimulation with release of neurotransmitters onto afferent nerves that innervate taste buds. In analogy to neurotransmitter release in other cells, it is expected that neurotransmitter release in taste cells is dependent on an increase in intracellular Ca2+ ([Ca2+]i). We have studied changes in [Ca2+]i elicited by the taste stimuli L- and D-arginine in isolated taste cells from the channel catfish (Ictalurus punctatus). In a sample of 119 cells, we found 15 cells responding to L-arginine, and 12 cells responding to D-arginine with an increase in [Ca2+]i. The response to L-arginine was inhibited by equimolar D-arginine in cells where D-arginine alone did not cause a change in [Ca2+]i, which is consistent with mediation of this response by a previously characterized L-arginine-gated nonspecific cation channel antagonized by D-arginine [31]. However, we also found that these taste stimuli elicited decreases in [Ca2+]i in substantial number of cells (6 for L-Arg, and 2 for D-Arg, n = 119). These observations suggest that stimulation of taste cells with sapid stimuli may result in simultaneous excitation and inhibition of different taste cells within the taste bud, which could be involved in local processing of the taste signal.

Gustatory thalamus lesions in the rat: I. Innate taste preferences and aversions.

Two experiments examined the innate taste preferences and aversions of rats with electrolytic lesions of the gustatory thalamus (GT). Contrary to previous research, GT lesions had only a minor influence on intake of the 4 basic tastes as assessed with the 24-hr, 2-bottle preference test in Experiment 1. The same lesioned rats, when tested with the same stimuli in the 15-min, single-bottle procedure in Experiment 2, showed normal consumption patterns except for sucrose intake, which was attenuated. The conflicting findings of previous and present research are considered to result from differences in lesion size. The current data suggest that the GT has a relatively minor functional role in the unconditioned acceptance or rejection of sapid stimuli.

Sodium-deficient diet reduces gustatory activity in the nucleus of the solitary tract of behaving rats.

The activity of single taste neurons was recorded from the nucleus of the solitary tract before (n = 41) and after (n = 58) awake, behaving rats were switched to a sodium-free diet. During sodium deprivation, the spontaneous activity of the neurons increased (142%), but responses to water and sapid stimuli decreased. For all neurons in the sample, the mean response to water decreased to 72% of its predeprivation level, NaCl dropped to 53%, sucrose to 41%, citric acid to 68%, and quinine HCl to 84%. Despite the drop in magnitude, the response profiles of the taste neurons were not changed by the dietary condition. In the Na-replete state, 61% of the activity elicited by NaCl occurred in NaCl-best cells and 33% in sucrose-best neurons. In the depleted state, these values were 60 and 26%, respectively. Nevertheless, at the highest concentrations tested, deprivation did alter the relative responsiveness of the gustatory neurons to sucrose and NaCl in specific categories of neurons. Compared with acute preparations, dietary sodium deprivation in awake, behaving rats produced a more general reduction in the gustatory responses of neurons in the nucleus of the solitary tract. The largest reductions in elicited activity occurred for the "best stimulus" of a particular neuron, thus leading to smaller differences in response magnitude across stimuli, particularly at the highest concentrations tested.

Concentration-dependent licking of sucrose and sodium chloride in rats with parabrachial gustatory lesions

The medial zone of parabrachial nuclei (PBN) serves as an obligatory synapse in the central gustatory system in rodents. Lesions in the PBN impair taste aversion learning and depletion-induced sodium appetite in rats, and also alter the ingestion of sapid stimuli. Interpretation of these lesion-induced behavioral deficits requires an evaluation of whether taste function is compromised. The present study examined whether rats with PBN lesions could show normal concentration-dependent changes in licking behavior to very small volumes of NaCl and sucrose. Physiological state was also varied; taste responsivity was examined in water-deprived and nondeprived rats. In a specially designed gustometer, nine rats with electrophysiologically guided lesions in the PBN and five surgical controls were trained to lick a drinking spout to receive 10-s access to various concentrations of NaCl (0.03–1.0 M) and sucrose (0.01–1.0 M) during 30-min sessions. Water-deprived control rats progressively decreased their responses compared with water as the concentration of NaCl was raised. In contrast, water-deprived PBNX rats did not decrease their licking responses to NaCl relative to water until the concentration reached 1.0 M. In the nondeprived state, control and PBNX rats decreased their responsiveness as a function of NaCl concentration, and the two groups did not differ. The licking responses of water-deprived PBNX rats did not differ from control rats when sucrose was the stimulus. In the nondeprived condition, both groups monotonically increased their licking to sucrose as a function of concentration, but PBNX rats were significantly less responsive than controls. These findings demonstrate that rats with lesions centered in the parabrachial gustatory area are not ageusic, but under certain physiological conditions these lesions do appear to blunt responsivity to sapid stimuli.

Gustatory responses of neurons in the nucleus of the solitary tract of behaving rats

1. The activity of 117 single neurons was recorded in the rostral nucleus of the solitary tract (NST) and tested with each of four standard chemical stimuli [sucrose, NaCl, citric acid, and quinine HCl (QHCl)] and distilled water in awake, behaving rats. In 101 of these neurons, at least one sapid stimulus elicited a significant taste response. The mean spontaneous rate of the taste neurons was 4.1 +/- 5.8 (SD) spike/s. The mean response magnitudes were as follows: sucrose, 10.6 +/- 11.7; NaCl, 8.6 +/- 14.6; citric acid, 6.2 +/- 7.8; and QHCl, 2.4 +/- 6.6 spikes/s. 2. On the basis of their largest response, 42 taste neurons were classified as sucrose-best, 25 as NaCl-best, 30 as citric acid-best, and 4 as QHCl-best. The mean spontaneous rates for these categories were 4.9 +/- 6.2 for sucrose-best cells, 5.8 +/- 7.4 for NaCl-best, 1.6 +/- 2.0 for citric acid-best, and 5.8 +/- 6.0 spikes/s for QHCl-best. The spontaneous rate of the citric acid-best neurons was significantly lower than that of the other categories. 3. At the standard concentrations, 45 taste cells (44.6%) responded significantly to only one of the gustatory stimuli. Of the 30 acid-best neurons, 23 (76.7%) responded only to citric acid. For sucrose-best cells, specific sensitivity was less common (18/42, 42.9%), and for NaCl-best neurons, it was relatively uncommon (3/25, 12%). One of the 4 QHCl-best neurons was specific. In a concentration series, more than one-half of the 19 specific neurons tested responded to only one chemical at any strength. 4. The mean entropy for the excitatory responses of all gustatory neurons was 0.60. Citric acid-best cells showed the least breadth of responsiveness (0.49), sucrose-best cells were somewhat broader (0.56), but NaCl-best and QHCl-best cells were considerably less selective (0.77 and 0.79, respectively). Inhibition was observed infrequently and never reached the criterion for significance. 5. In the hierarchical cluster analysis, the four largest clusters segregated neurons primarily by best-stimulus category. The major exception to this was a group of sucrose-best neurons that also responded to NaCl and were grouped with the NaCl-best neurons. In a two-dimensional space, the specific taste neurons, those that responded to only one of the four standard sapid stimuli, remained in well-separated groups. These specific groups, however, were joined in a ring-like formation by other neurons that responded to more than one of the sapid stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Parabrachial gustatory neural activity during licking by rats

1. A total of 51 single neurons was recorded from the pontine parabrachial nuclei of three rats being given sapid stimuli either via intraoral infusions or during spontaneous licking behavior. In 46 neurons, sapid stimuli elicited significant taste responses; of these, 28 responded best to NaCl, 15 to sucrose, 2 to citric acid, and 1 to quinine HCl. The remaining five neurons responded significantly only to water. The mean spontaneous rate of taste neurons during the intraoral infusion and licking sessions was 11.1 +/- 1.1 and 10.8 +/- 1.2 (SE) spikes/s, respectively. 2. Of the 39 neurons tested during both licking and intraoral infusions, four responded significantly only to water via either route. The remaining 35 neurons responded significantly to at least some sapid stimuli. The best-stimulus categories remained the same regardless of the route of fluid delivery (24 NaCl best, 10 sucrose best, 1 citric acid best). When the rats were licking the stimuli, nine taste neurons responded significantly to only one sapid chemical [6 Na specific (Ns) and 3 sucrose specific (Ss)] but were more broadly tuned during intraoral infusions. Conversely, three taste neurons that responded specifically during intraoral infusions (3 Na specific) were not as specific when the animal licked the same fluids. 3. Thirty-five taste neurons were tested via both stimulus routes. These data were compared in three ways. First, for each neuron, the responses elicited during licking and intraoral infusions were compared for each of the four standard sapid stimuli. The Pearson correlation coefficients for the 35 taste neurons ranged from 0.9997 to 0.6785, with a mean at 0.953 +/- 0.012 (SE). The second comparison was between stimulus routes across chemicals. With the use of raw responses, the correlation coefficients for NaCl, sucrose, citric acid, and QHCl ranged from 0.925 to 0.778 (t test, P less than 0.0001). With the activity elicited by water subtracted (corrected responses), the correlation coefficients for NaCl, sucrose, citric acid, and QHCl were 0.900, 0.795, 0.369, and 0.211, respectively. The coefficient for QHCl was not significant (t test, P greater than 0.05). Finally, the mean responses to NaCl, sucrose, and citric acid delivered by both routes were compared and found not to differ (paired t test, P greater than 0.05). 4. In separate hierarchical cluster analyses for the licking and infusion data, the largest cluster in each contained all of the Na-best neurons and the next largest, all of the sucrose-best cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Preference of old world monkeys for amino acids and other gustatory stimuli: The influence of monosodium glutamate

Monosodium glutamate (MSG) is widely considered to enhance the flavor of beef, chicken, fish, and vegetables. This effect may be due to the interaction of glutamate with free amino acids or other basic taste stimuli present in these foods. A single-bottle test was used in order to test the preference of Old World monkeys for an extended array of gustatory stimuli individually and in combination with MSG. Six male cynomolgus monkeys, maintained on an 18-h water deprivation schedule, were given 30 min access daily to a sapid stimulus or distilled water. The following stimuli (selected on the basis of prior experimentation) were tested alone and in combination with 0.03 M MSG: sucrose, fructose, glucose, maltose, polycose, sodium saccharin, glycine, sodium chloride, hydrochloric acid, tartaric acid, malic acid, citric acid, quinine hydrochloride, urea, and beef broth. The L-isomers of the following free amino acids also were tested: alanine, histidine, phenylalanine, proline, serine, valine. The addition of MSG to the stimuli listed above had no significant effect upon the monkeys' preference or aversion thresholds. Most suprathreshold stimuli that the monkeys neither preferred nor avoided were unaffected by the addition of MSG. The monkeys' preference for sugars was adversely affected in mixtures containing MSG, but other stimuli that humans report to be sweet tasting (alanine, glycine, polycose) were unaffected. The data from the present experiment demonstrate that MSG was capable of altering the monkeys' preference for some but not all of the gustatory stimuli tested. Because MSG did not enhance the monkeys' preference for the basic taste stimuli or free amino acids, the mechanism by which MSG enhances the taste of beef, chicken, and fish in humans remains unclear.