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PubMed2002

The meninges contribute to the conditioned taste avoidance induced by neural cooling in male rats.

After consumption of a novel sucrose solution, temporary cooling of neural areas that mediate conditioned taste avoidance can itself induce conditioned avoidance to the sucrose. It has been suggested that this effect is either a result of inactivation of neurons in these areas or of cooling the meninges. In a series of studies, we demonstrated that cooling the outer layer of the meninges, the dura mater, does not contribute to the conditioned taste avoidance induced by cooling any of these areas. The present experiments were designed to determine whether the inner layers of the meninges are involved. If they are involved, then one would expect that cooling locations in the brain that do not mediate conditioned taste avoidance, such as the caudate putamen (CP), would induce conditioned taste avoidance as long as the meninges were cooled as well. One also would expect that cooling neural tissue without cooling the meninges would reduce the strength of the conditioned taste avoidance. Experiment 1 established that the temperature of the neural tissue and meninges around the cold probes implanted in the CP were cooled to temperatures that have been shown to block synaptic transmission. Experiment 2 demonstrated that cooling the caudate putamen and overlying cortex and meninges induced conditioned taste avoidance. In experiment 3, a circle of meninges was cut away so that the caudate putamen and overlying cortex could be cooled without cooling the meninges. The strength of the conditioned taste avoidance was substantially reduced, but it was not entirely eliminated. These data support the hypothesis that cooling the meninges contributes to the conditioned taste avoidance induced by neural cooling. They also allow the possibility that neural inactivation produces physiological changes that can induce conditioned taste avoidance.

Animals↗

PubMed2003

Sweet taste and blood pressure-related analgesia.

To test the prediction that sweet taste modifies responses to cold induced pain, 72 young adults held sweet, bitter and water solutions in their mouths, in counterbalanced order, before and during a cold pain stimulus. To test whether or not blood pressure interacts with sweet taste analgesia, measurements of resting blood pressure were also obtained. A significant main effect of taste on pain tolerance was observed, as well as a significant interaction between resting mean arterial pressure (MAP) and taste on tolerance. Sweet taste was associated with a prolongation of tolerance compared to the bitter and water conditions. When participants were split along the median for MAP, sweet taste was associated with an 18.1% increase in pain tolerance compared with water for those with lower MAP. No significant impact of taste on pain sensitivity was observed among participants with higher MAP. Groupwise comparisons revealed a significant difference in pain tolerance between participants with higher and lower MAP in the water condition but not in the sweet condition, replicating previous findings of a reduced sensitivity to pain among those with higher blood pressure. The analgesic effects of sweet tasting solutions seen previously in human infants and children may also be present in adults. Individuals with higher blood pressure may not be as sensitive to the presumably opioid-mediated analgesic effects of sweet taste, perhaps due to opioid dysregulation.

Adult↗

PubMed2003

Development of oral acetaminophen chewable tablets with inhibited bitter taste.

Various formulations with some matrix bases and corrigents were examined for development of oral chewable tablets which suppressed the bitter taste of acetaminophen, often used as an antipyretic for infants. Corn starch/lactose, cacao butter and hard fat (Witepsol H-15) were used for matrix bases, and sucrose, cocoa powder and commercial bitter-masking powder mixture made from lecithin (Benecoat BMI-40) were used for corrigents against bitter taste. The bitter taste intensity was evaluated using volunteers by comparison of test samples with standard solutions containing quinine at various concentrations. For the tablets made of matrix base and drug, Witepsol H-15 best inhibited the bitter taste of the drug, and the bitter strength tended to be suppressed with increase in the Witepsol H-15 amount. When the inhibitory effect on the bitter taste of acetaminophen solution was compared among the corrigents, each tended to suppress the bitter taste; especially, Benecoat BMI-40 exhibited a more inhibitory effect. Further, chewable tablets were made of one matrix base and one corrigent, and of one matrix base and two kinds of corrigents, their bitter taste intensities after chewing were compared. As a result, the tablets made of Witepsol H-15/Benecoat BMI-40/sucrose, of Witepsol H-15/cocoa powder/sucrose and of Witepsol H-15/sucrose best masked the bitter taste so that they were tolerable enough to chew and swallow. The dosage forms best masking bitter taste showed good release of the drug, indicating little change in bioavailability by masking.

Acetaminophen↗

PubMed2002

Naltrexone modifies the palatability of basic tastes and alcohol in outbred male rats.

Naltrexone, an opioid antagonist, has been shown to reduce the palatability of 10% alcohol solutions in rats, as measured by taste reactivity. In the present study, the effect of acute naltrexone treatment on taste reactivity to a variety of taste solutions and concentrations was tested to determine whether naltrexone has generalized effects on taste responsiveness. Thirty minutes before a taste reactivity test, rats were injected with either naltrexone (3 mg/kg; n = 15) or saline (n = 15). On separate days, rats were tested with distilled water and three concentrations each of sucrose (0.1, 0.5, and 1.0 M), sodium chloride (0.06, 0.10, and 0.30 M), quinine hydrochloride (0.0005, 0.001, and 0.005 M), and alcohol [10%, 20%, and 40% (vol./vol.)]. In Experiment 1, naltrexone consistently reduced the palatability of alcohol and sodium chloride solutions (across concentrations), as reflected by a decrease in ingestive responding and an increase in aversive responding. Naltrexone increased aversive responding for sucrose but did not affect ingestive responding for these solutions. Finally, there was no significant effect of naltrexone on responding to quinine hydrochloride. A second experiment with naive rats and five concentrations of sucrose (0.01, 0.05, 0.1, 0.5, and 1.0 M) replicated the initial data: Across concentrations, naltrexone produced a significant increase in aversive responding but did not alter ingestive responding. In Experiment 3, naive rats were tested with five concentrations of quinine hydrochloride (0.00001, 0.00005, 0.0001, 0.0005, and 0.005 M). Results indicated that naltrexone significantly altered taste reactivity to the bitter solutions (less ingestive responding and more aversive responding), particularly at the lower concentrations. The results indicate that naltrexone treatment has significant effects on taste reactivity to some aqueous solutions (alcohol, sodium chloride), regardless of solution concentration. The effects of naltrexone on sucrose and quinine reactivity are more difficult to describe because the drug effects seemed to be dependent on the specific measure examined (ingestive vs. aversive responses) and the concentration of the solution. These results support the suggestion that naltrexone has a fairly generalized effect on taste reactivity to taste solutions; specifically, naltrexone seems to make solutions more aversive, as revealed by a decrease in ingestive responding and an increase in aversive responding.

Alcohol Drinking↗

PubMed2000

Elevated and sustained desire for sweet taste in african-americans: a potential factor in the development of obesity.

Oral habituation is a relatively long-lasting decrease in oral responsiveness that results from the repeated presentation of a single stimulus. The purpose of this study was to evaluate the degree of habituation to sweet-tasting foods and to determine whether there are differences in the rate of habituation between African Americans and European Americans. These two groups were compared because the prevalence of obesity and obesity-related disorders such as diabetes and hypertension is significantly higher among African Americans than among European Americans. Nine different commercial foods and beverages that differed in sweetness intensity and caloric density served as stimuli. Subjects tasted and rated each food once per minute for a 30-min period on scales related to desire for another taste of the same sample and desire for a different taste. The stimuli and portion size for each of the 30 samples were two candy bars (Ultra Slim-Fast Cocoa Almond Crunch Bar, 1/16 of a bar; Natural Nectar Peanut Butter Granola Bar, 1/16 of a bar), three beverages (Nestea Lemon Flavored Instant Tea with NutraSweet, 5 mL; Welch's Grape Juice, 5 mL; Pink Swimmingo Kool-Aid, 5 mL), two gelatin desserts (Cherry Flavored Jell-O Gelatin, 5 g; Cherry Flavored Jell-O Gelatin with NutraSweet, 5 g), one enteral nutrition drink (Vanilla Ensure Plus, 5 mL), and one pudding (Ultra Slim-Fast Chocolate Pudding, 5 g). Subjects consumed the entire portion of each sample. Habituation occurred for seven of the nine foods as judged by a decrease in the desire for another taste of the same food. The degree of habituation for European Americans and African Americans was similar except for the sweetest food (Cherry Flavored Jell-O Gelatin with NutraSweet), for which African Americans showed no habituation. The degree of habituation in both groups was unrelated to caloric density. Overall, young African Americans had a significantly greater desire for another taste of the same food than did young European Americans for seven of the nine foods, and this desire was strongly correlated with the sweetness intensity for young African Americans but not for young European Americans. Furthermore, young African Americans had a greater desire than young European Americans for a different taste for seven of nine foods. The greater desire for intense sweet tastes may be a factor in the elevated incidence of obesity and diabetes in African Americans. In addition, young African Americans had greater perceived stress in this study than did young European Americans. If African Americans use sweet taste to compensate for feelings of stress, this compensation may also contribute to weight gain.

Adult↗

PubMed2003

Cholinergic dependence of taste memory formation: evidence of two distinct processes.

Learning the aversive or positive consequences associated with novel taste solutions has a strong significance for an animal's survival. A lack of recognition of a taste's consequences could prevent ingestion of potential edibles or encounter death. We used conditioned taste aversion (CTA) and attenuation of neophobia (AN) to study aversive and safe taste memory formation. To determine if muscarinic receptors in the insular cortex participate differentially in both tasks, we infused the muscarinic antagonists scopolamine at distinct times before or after the presentation of a strong concentration of saccharin, followed by either an i.p. injection of a malaise-inducing agent or no injection. Our results showed that blockade of muscarinic receptors before taste presentation disrupts both learning tasks. However, the same treatment after the taste prevents AN but not CTA. These results clearly demonstrate that cortical cholinergic activity participates in the acquisition of both safe and aversive memory formation, and that cortical muscarinic receptors seem to be necessary for safe but not for aversive taste memory consolidation. These results suggest that the taste memory trace is processed in the insular cortex simultaneously by at least two independent mechanisms, and that their interaction would determine the degree of aversion or preference learned to a novel taste.

Animals↗

PubMed2003

Co-expression pattern of Shh with Prox1 and that of Nkx2.2 with Mash1 in mouse taste bud.

In mammals, taste buds are maintained by continuous turnover of cells, even in adulthood. Cell proliferation and differentiation continue to produce taste cells, which express various genes related to taste reception. We found the co-expression of Sonic hedgehog (Shh) with Prox1 and that of Nkx2.2 with Mash1 in adult mouse taste buds. Whereas Prox1was expressed strongly in cells in the basal region of mouse taste buds where Shh was co-expressed, it was expressed weakly in almost all taste bud cells lacking Shh expression. At 0.5 day after birth, when taste cells have not yet differentiated, the expressions of Shh and Prox1 completely overlapped in the epithelium of circumvallate papillae. Nkx2.2 was observed in cells expressing Mash1, but not in cells expressing genes related to taste reception, such as gustducin and T1R3. Almost all fusiform cells expressing Mash1 co-expressed Nkx2.2, while the majority of round cells expressing Mash1 in the basal region of taste buds lacked Nkx2.2 expression.

Animals↗

PubMed1988

Intraoral intake and taste reactivity responses elicited by sucrose and sodium chloride in chronic decerebrate rats.

The oral stimulating effects of sucrose and sodium chloride (NaCl) were assessed in chronic decerebrate and pair-fed intact control rats by measuring both oral motor taste-reactivity responses and intraoral intake volume. Taste-reactivity responses were videotaped during the first minute of the intraoral taste infusion. The infusion continued until the taste solution was rejected from the mouth, and the intake volume was computed accordingly. The number of ingestive taste-reactivity responses and the volume of intraoral intake consumed by pair-fed control and decerebrate rats increased with increasing sucrose concentration. Sucrose intake increased as concentration increased to 0.1 M, then plateaued between 0.3, 1.3, and 2.0 M sucrose for both groups. For control rats, intraoral NaCl elicited an inverted U-shaped function for both taste-reactivity responses and intake. Taste-reactivity responses of chronic decerebrate rats varied with NaCl concentration. In contrast to control rats, intake of NaCl did not differ from that of water for decerebrate rats. These data indicate that caudal brain-stem mechanisms are sufficient to control sucrose intake but are not adequate for the concentration dependent intake of NaCl. Second, these data also indicate that it is possible for taste-elicited oral motor responses to be dissociated from intake. The different roles of taste and postingestive factors in sucrose and NaCl intake are discussed.

Animals↗

PubMed1977

Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

Rats lacking gustatory neocortex (n = 24) and normal rats (n = 24) were familiarized to either hydrochloric acid (10(-1.6) M) or quinine hydrochloride (10(-4) M) solutions during free-drinking trials. They were trained subsequently to avoid either the familiar or the novel taste stimulus, using a balanced design, by pairing the to-be-associated taste with ip injections of apomorphine hydrochloride. Balanced, nonpaired presentations of the other taste solution and water were presented also. Normal rats more efficiently learned to avoid the novel compared with the familiar taste. Rats with gustatory neocortex lesions did not differentiate novel from familiar tastes. They learned aversions to both in a manner highly similar to the aversion learning of familiar tastes by the normal group. Therefore, rats lacking gustatory neocortex displayed an associative deficiency, relative to normal, only when they were trained on novel stimuli. This observation supports an earlier suggestion that gustatory neocortex lesions disrupt the conditionability of taste stimuli by reducing or eliminating responses to taste novelty. This suggestion is supported further by the absence of a "neophobic" response in the operated rats to the first presentation of a taste stimulus.

Animals↗

PubMed1982

Contribution of the rat's neocortex to ingestive control: I. Latent learning for the taste of sodium chloride.

Neocortical mechanisms do not directly contribute to the execution of taste discrimination, sodium appetite, or the acquisition of a taste aversion in the rat. Examination of previous studies led to the question of whether some permanent ingestive control deficit would be revealed if elements of these experimental paradigms were combined. A latent learning paradigm for the taste of salt was applied to decorticate rats. The ability of decorticate rats to associate how they obtained the taste of NaCl when sodium replete was assessed by examining bar presses during extinction when sodium depleted. Intact rats exposed to 4-6 hr of NaCl taste training retained the association after decortication; decorticate rats exposed to the same training acquired the association. What was most striking was that decorticate rats exposed to as little as 2 min of NaCl taste training demonstrated the ability to associate bar pressing with NaCl by their resistance to extinction. The association was specific to NaCl training; training with distilled water or KCl did not yield resistance to extinction during sodium depletion. Subcortical structures are therefore adequate for latent learning involving NaCl taste. Conversely, data of other investigators have revealed that the neocortex is required for the retention of taste aversion learning for the same taste.

Animals↗

PubMed1995

Coupling of bitter receptor to phosphodiesterase through transducin in taste receptor cells.

The rod and cone transducins are specific G proteins originally thought to be present only in photoreceptor cells of the vertebrate retina. Transducins convert light stimulation of photoreceptor opsins into activation of cyclic GMP phosphodiesterase (reviewed in refs. 5-7). A transducin-like G protein, gustducin, has been identified and cloned from rat taste cells. We report here that rod transducin is also present in vertebrate taste cells, where it specifically activates a phosphodiesterase isolated from taste tissue. Furthermore, the bitter compound denatonium in the presence of taste-cell membranes activates transducin but not Gi. A peptide that competitively inhibits rhodopsin activation of transducin also blocks taste-cell membrane activation of transducin, arguing for the involvement of a seven-transmembrane-helix G-protein-coupled receptor. These results suggest that rod transducin transduces bitter taste by coupling taste receptor(s) to taste-cell phosphodiesterase. Phosphodieterase-mediated degradation of cyclic nucleotides may lead to taste-cell depolarization through the recently identified cyclic-nucleotide-suppressible conductance.

Animals↗

PubMed1993

Identification of electrophysiologically distinct cell subpopulations in Necturus taste buds.

We used the patch clamp technique to record from taste cells in thin transverse slices of lingual epithelium from Necturus maculosus. In this preparation, the epithelial polarity and the cellular organization of the taste buds, as well as the interrelationships among cells within the taste bud, were preserved. Whole-cell recording, combined with cell identification using Lucifer yellow, allowed us to identify distinct subpopulations of taste cells based on their electrophysiological properties. Receptor cells could be divided in two groups: one group was characterized by the presence of voltage-gated Na+, K+, and Ca2+ currents; the other group was characterized by the presence of K+ currents only. Therefore, receptor cells in the first group would be expected to be capable of generating action potentials, whereas receptor cells in the second group would not. Basal taste cells could also be divided into two different groups. Some basal cells possessed voltage-gated Na+, K+, and Ca2+ conductances, whereas other basal cells only had K+ conductance. In addition to single taste cells, we were able to identify electrically coupled taste cells. We monitored cell-cell coupling by measuring membrane capacitance and by observing Lucifer yellow dye coupling. Electrical coupling in pairs of dye-coupled taste receptor cells was strong, as indicated by experiments with the uncoupling agent 1-octanol. Electrically coupled receptor cells possessed voltage-gated currents, including Na+ and K+ currents. The electrophysiological differentiation among taste cells presumably is related to functional diversifications, such as different chemosensitivities.

Action Potentials↗

PubMed1996

Neuromodulation of transduction and signal processing in the end organs of taste.

Chemical synapses transmit gustatory signals from taste receptor cells to sensory afferent axons. Chemical (and electrical) synapses also provide a lateral pathway for cells within the taste bud to communicate. Lateral synaptic pathways may represent some form of signal processing in the peripheral end organs of taste. Efferent synaptic input may also regulate sensory transduction in taste buds. To date, the synaptic neurotransmitter(s) or neuromodulator(s) released at chemical synapses in taste buds have not been identified unambiguously. This paper summarizes the attempts that have been made over the past 40 years to identify the neuroactive substances acting at taste bud synapses. We review the four traditional criteria for identifying chemical transmitters elsewhere in the nervous system-localization, uptake/degradation, release and physiological actions- and apply these criteria to neuroactive substances in taste buds. The most complete evidence to date implicates serotonin as a neuromodulator of taste transduction in the end organs. However, studies also suggest that adrenergic, cholinergic and peptidergic neurotransmission may be involved in taste buds.

Animals↗

PubMed2000

Selective removal of a target stimulus localized by taste in humans.

Recent studies have shown that people can localize a punctate gustatory stimulus on the lingual epithelium in the absence of discriminative tactile cues. The present studies examined the human ability to localize taste sensations on the tongue and to use this information to remove selectively a target stimulus (a flavored, 1 cm(3) gelatin cube) from the mouth when presented with non-target distractors that vary in number and taste. Findings indicate that humans are capable of localizing and removing either an aversive or an appetitive gustatory target from a field of tactile distractors via taste sensations alone, although this ability diminishes as the number of distractors increases (implicating serial searches, rather than parallel). In addition, humans can localize and selectively remove a target taste in the presence of distractors of another distinct taste quality. Under these conditions performance is either unaffected or reduced, which indicates that contrast with the distinct taste of the distractors does not enhance performance. Humans also are capable of removing a nearly tasteless cube from a field of flavored distractors, but this is clearly a more difficult task, suggesting that 'tactile capture' of taste occurs for the tasteless target cube and interferes with the localization of taste. Finally, perceived suprathreshold stimulus intensity did not seem to be related to the ability to localize and remove a target stimulus via taste sensations and failed to account for variations in performance across individuals.

Adolescent↗

PubMed2000

Taste preference synergy between glutamate receptor agonists and inosine monophosphate in rats.

Monosodium glutamate (MSG) elicits a taste called umami and interacts synergistically with nucleotide monophosphates such as 5'-inosine monophosphate (IMP) to potentiate this taste intensity. Indeed, the synergistic interaction of nucleotide monophosphates and MSG is a hallmark of umami. We examined interactions between MSG and other taste stimuli, including IMP, by measuring the lick rates of non-deprived rats during 30 s trials. To control for non-linear psychophysical functions, the concentration of one taste stimulus in a binary mixture was systematically increased while the concentration of the second taste stimulus was decreased (stimulus substitution method). Synergy between two stimuli was detected if the lick rate for a binary mixture exceeded that expected from the sum of the lick rates for each stimulus alone. In initial experiments, taste synergy was observed when rats were presented with mixtures of MSG and IMP but not with mixtures of MSG and sucrose. In subsequent experiments, glutamate receptor agonists other than MSG were presented with IMP to test for taste synergy. No evidence of synergy was seen when rats were presented with mixtures of IMP and kainic acid or IMP and N:-methyl-D-aspartate. However, taste synergy between IMP and L-AP4, a potent agonist at mGluR4 receptors, was observed. These results suggest that a metabotropic glutamate receptor similar to mGluR4 may be involved in the taste synergy that characterizes umami.

Animals↗

PubMed2002

Virus-mediated transfer of foreign DNA into taste receptor cells.

Foreign genes can be transferred into taste cells via adenoviral vectors. The present study was undertaken to characterize the subpopulation of taste cells that are susceptible to adenovirus infection and to determine whether another viral vector, derived from herpes simplex 1 (HSV-1), infects the same subpopulation of taste cells. Using an adenovirus containing the gene for enhanced green fluorescent protein (EGFP) under the control of the human cytomegalovirus (CMV) immediate early promoter, we found that EGFP was present in blood group antigen H immunoreactive (ir) taste cells, but not in gustducin-ir or PGP 9.5-ir cells. Infection of taste buds with an HSV-1 vector containing EGFP also resulted in a subpopulation of EGFP-positive taste cells. However, both gustducin-ir and PGP 9.5-ir taste cells expressed the marker protein. In conclusion, this study shows that both adenoviral and HSV-1 vectors can be used to transfer foreign genes into the cells of isolated rat taste buds and that different viruses can be used to target specific subpopulations of taste cells.

Adenoviridae↗

PubMed1986

Quantitative anatomical study of taste buds in fungiform papillae of young and old Fischer rats.

To determine if differences in neural taste responses relate to taste bud loss in old age, taste buds were counted in fungiform papillae of Fischer 344 rats aged 4 to 6 months, 20 to 24 months, and 30 to 37 months. Papillae anterior to the intermolar eminence on one half of the tongue were examined in serial sections. Presence or absence of a taste bud was noted and taste bud diameter was measured. Average percentages of papillae that contained a taste bud in the three groups were 99.6, 99.3, and 94.7%. This is a significant age-related difference but actual number of taste buds lost in the oldest rats was small. Taste bud diameter did not differ with age and general anatomical characteristics of buds were similar in all groups. Thus, anatomical observations on taste bud maintenance in rats over a wide age range, coupled with neurophysiological data, demonstrate that the integrity of the peripheral gustatory system is not altered greatly in old age.

Aging↗

PubMedDate not supplied

Taste memory induces brain activation as revealed by functional MRI.

PURPOSE: Our goal was to use functional MRI (fMRI) to measure brain activation in response to imagination of tastes in humans. METHOD: fMR brain scans were obtained in 31 subjects (12 men, 19 women) using multislice FLASH MRI and echo planar imaging (EPI) in response to imagination of tastes of salt and sweet in coronal sections selected from anterior to posterior temporal brain regions. Activation images were derived using correlation analysis, and ratios of areas of brain activated to total brain areas were calculated. Total activated pixel counts were used to quantitate regional brain activation. RESULTS: Activation was present in each section in all subjects after imagination of each tastant. Activation was similar in response to imagination of either salt or sweet and was quantitatively similar to that previously reported in response to imagination of odors of banana and peppermint. Activation was similar in both men and women as opposed to previous results of odor memory in which activation in men was greater than in women. However, subjective responses of intensity of imagined tastes were significantly greater than those previously obtained for odor memory and were consistently, albeit not significantly, greater in women than in men, similar to results previously reported for odor memory. Brain regions activated in response to taste imagination were consistent with regions previously described as involved with actual taste perception in both humans and animals. Regional brain localization for salt and sweet memories could not be differentiated. CONCLUSION: These studies indicate that (a) tastes can be imagined, (b) brain regions activated for taste imagination are consistent with regions previously described for actual taste perception, and (c) similar to odor memory for banana and menthone, regional brain localization for salt or sweet taste memories could not be differentiated.

Adult↗