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At least 595 records · Page 33Linked to original sources
PubMed1991

The role of substance P and calcitonin gene-related peptide containing nerve fibers in maintaining fungiform taste buds in the rat after a chronic chorda tympani nerve injury.

Taste buds in the anterior part of the tongue of adult rats were denervated by unilateral resection of the chorda tympani nerve in the middle ear. Three months later one group of animals was perfused and their tongues were processed for demonstration of substance P (SP) and calcitonin gene-related peptide (CGRP) immunoreactivity. Fungiform taste buds found on the denervated side showed increased numbers of intragemmal SP- and CGRP-immunoreactive (IR) fibers compared to the normal side. Compared to the normal side, the number of taste buds appeared to be fewer on the denervated side. Moreover, taste buds on this side seemed to be only partially restored. Another group of animals was given the neurotoxin capsaicin which causes a depletion of SP and CGRP from sensory axons. The animals were perfused 2 or 3 weeks after the capsaicin treatment, and their tongues prepared for SP and CGRP immunohistochemistry or for histological examination of taste buds. Very few SP- and CGRP-IR fibers were present in capsaicin-treated animals. In these animals almost all fungiform taste buds and papillae on the chorda tympani-injured side disappeared. In contrast, normal numbers of taste buds were still present on the contralateral side where the chorda tympani innervation remained intact. It is conceivable that taste buds on the chorda tympani-innervated part of the tongue, deprived of the normal chorda tympani-innervation, can regenerate and become reinnervated by SP- and CGRP-containing fibers, and that these are essential for partially restoring and maintaining the structure of the denervated taste buds and the fungiform papillae.

Animals↗
PubMed1985

Taste discriminations in rats lacking anterior insular gustatory neocortex.

Previous neurobehavioral investigations have demonstrated that the anterior insular gustatory neocortex (AIGN) mediates taste-illness learning. The present experiment evaluated taste discriminations in rats lacking AIGN. Two groups of rats received distinct surgical treatments. One-half of the animals received bilateral electrolytic lesion placements in the AIGN: Remaining animals received anesthesia and scalp incisions only. Following postoperative recovery animals received standard two-bottle preference tests with various concentrations of sucrose to evaluate gustatory reactivity. Animals thereafter received two-bottle discrimination tests with selected sucrose concentrations. At the conclusion of preference tests and discrimination tests with sucrose, preference tests and discrimination tests were conducted with sodium chloride. Following those tests animals received taste aversion conditioning to determine whether or not AIGN lesions impaired taste-illness learning. Results of two-bottle taste tests indicated that AIGN lesions do not obviously alter taste reactivity nor taste discriminations to preferred concentrations of sucrose and NaCl. Anterior insular lesions did, however, impair normal taste aversion learning. These results, in combination with those of previous investigators, provide further evidence that the AIGN preferentially contributes to taste learning functions.

Animals↗
PubMed1992

Effects of body weight loss and taste on VMH-LH electrical activity of rats.

Electrical responses of ventromedial (VMH) and lateral (LH) hypothalamus to graded decrease in body weight and to taste were recorded from a conscious rat with chronically implanted macroelectrodes. Graded reduction in body weight was correlated with gradual increase in LH activity and reciprocal decrease in VMH activity, both of which were stable and specific to each gradation in body weight. On gustation of any test solution, basal activity was temporarily altered, if any. On sweet taste of calorically rich sucrose, VMH activity was enhanced and LH showed decrease. But on sweet taste of calorically inert saccharin, VMH activity was increased, though a reciprocal decrease in LH was not shown. Contrastingly, both bitter taste and salt taste caused increased LH activity but no change in VMH activity. Enhanced VMH activity correlated with sweet taste may be due to activation of VMH glucoreceptors. LH activation correlated with bitter and salt taste is a likely response of two distinct groups of LH units; one responding to salt taste and the other to bitter aversive taste.

Animals↗
PubMed1995

Taste quality profiles for fifteen organic and inorganic salts.

Biophysical studies of isolated taste receptor cells show that one transduction mechanism for Na+ salts involves the inward movement of Na+ through an apical ion channel, which is sensitive to the diuretic amiloride. An additional paracellular pathway also appears to be involved in NaCl transduction, but not in the transduction of organic Na+ salts. Little is known, however, about how these receptor mechanisms relate to taste perception. Recent human psychophysical studies suggest that the amiloride-sensitive transduction pathway is coupled to the sour side taste of these salts rather than to their saltiness. In the present study, we employed direct magnitude estimation of taste intensity and quality of fifteen organic and inorganic Na+, Li-, K+, and Ca+2 salts. Many salts had multiple taste qualities, such as the salty and bitter tastes of NH4Cl and KCl; the Ca+2 salts were predominantly bitter. Taste quality often changed with stimulus concentration. Multivariate analyses of their taste profiles resulted in a grouping of these 18 stimuli within a taste space bounded by NaCl, sucrose, citric acid, and QHCl, with the organic salts positioned between NaCl and citric acid. The organic Na+ salts and the Li+ salts were considerably less salty and proportionately more sour than NaCl. These results, combined with previous work showing that amiloride suppresses the sourness of NaCl and Na-gluconate, predict that the organic Na+ salts and the Li+ salts would be more greatly suppressed by amiloride treatment than would NaCl.

Adult↗
PubMed1996

An ear for quality: differential associative characteristics of taste-potentiated auditory and odor avoidance.

This research compared the avoidance behavior of rats exposed to either a taste-tone (NaCl-70 dB, 1800 Hz) or a taste-odor (NaCl-almond) compound that had been paired with LiCl-induced illness. When tested in the presence of either the odor or the auditory cue presented alone it was found that taste potentiated both cues, but stronger initial avoidance and resistance to extinction was shown to the odor cue. A second experiment examined the generalization of potentiated odor and auditory aversions to a novel environment. Rats were exposed to either a taste-odor or taste-tone compound, again followed by illness. Half of each group was tested in the conditioning chamber and half in a novel chamber. Odor aversions were not affected by location, whereas auditory aversions were significantly stronger in the conditioning chamber. Experiment 3 showed that taste-potentiated odor and auditory aversions showed different patterns of extinction when the taste aversion on which they were based was gradually extinguished. These experiments provide evidence that while the taste potentiation of auditory cues is a reliable phenomena, the pattern of effects is different from that of taste-potentiated odor aversions.

Acoustic Stimulation↗
PubMed1990

Perception and hedonics of sweet and fat taste in smokers and nonsmokers following nicotine intake.

Nicotine's effects on reducing perception and/or hedonics of sweet and fat taste may lead to less intake of sweet tasting, high-fat foods by smokers, helping to explain their generally lower body weights. Smokers and nonsmokers (n = 10 males each) rated perception (intensity and sensitivity) and hedonics (liking) of sweet/fat taste in milk samples varying both in sucrose (0, 5, 10, 20% w/w) and fat (0.1, 3.5, 11.7, 37.6% w/w) concentration on two occasions, once following intermittent presentation of nicotine (15 micrograms/kg) via measured dose nasal spray and the other following placebo. Nicotine significantly reduced perceived intensity of fat but not sweet taste and had no effect on sensitivity to either taste. There was no effect of nicotine on hedonics of sweet/fat taste. On the other hand, although there were no differences between smokers and nonsmokers in perception of sweet or fat, hedonics of sweet/fat taste was reduced in smokers regardless of nicotine or placebo intake. Thus, nicotine may acutely decrease fat taste perception without influencing sweet/fat hedonics, while long-term exposure (i.e., being a smoker) may produce chronically decreased taste hedonics without altering perception.

Adolescent↗
PubMed1991

Modulation of taste affect by hunger, caloric satiety, and sensory-specific satiety in the rat.

Human judgements of the pleasure of sweetness have been reported to be modulated by caloric hunger, satiety, and sensory-specific satiety. This study examined both hedonic and aversive facial/somatic reactions to taste in the rat, in order to confirm the relation of hunger and satiety to taste affect, and to assess whether affective modulation depends upon the cognitive factors that mediate human self-interpretation of affect. In the first experiment, the affective reactions of rats to sweet, bittersweet, and water tastes were assessed in five states of caloric hunger or satiety. Caloric satiety reduced positive hedonic reactions below normal levels. Conversely, 48-h food deprivation (but not 24-h deprivation) increased hedonic reactivity. Hedonic enhancement by hunger was not restricted to sweet tastes, but also extended to the palatability of water. Only the hedonic reactions to taste were changed by hunger or satiety: taste aversion was not altered. The second experiment compared the magnitude of affective change during sensory-specific satiety and caloric satiety. Taste-reactivity elicited by sucrose solution or milk was assessed after satiating meals of each of those foods. Sensory-specific satiety further reduced hedonic reactions below the level achieved by caloric satiety alone. Both for caloric satiety and for sensory-specific satiety changes in affect were restricted to positive hedonic reactions: no increase in aversion accompanied the hedonic decrements. These results confirm that taste affect is modulated during caloric hunger, caloric satiety, and sensory-specific satiety. In addition they indicate that the modulation of taste affect by hunger and satiety is confined to the positive limb of the two dimensions (hedonic vs. aversive) of palatability.

Affect↗
PubMed1976

Sugar binding to purified fractions from bovine taste buds and epithelial tissue. Relationships to bioactivity.

Binding of various sugars was compared in purified subfractions of taste buds isolated from bovine circumvallate papillae and of non-taste bud-bearing epithelium isolated from tissue surrounding these papillae. Binding of 14C-labeled sugars was greater in purified subfractions obtained from taste bud than from non-taste bud-bearing tissue and was, in general, greater in those taste bud subfractions in which a greater membrane purification was achieved. Binding specificity of the 14C-labeled sugars sucrose, fructose, glucose and of 14C-labeled cyclamate and saccharine was measured by competition of each 14C-labeled sugar or synthetic sweetener with its unlabeled homologous sugar in P4(B) taste bud subfractions; this binding, as shown for sucrose, was reversible and temperature dependent. Essentially no competition of the 14C-lageled sugars sucrose, fructose, glucose or 14C-labeled cyclamate and saccharine by their respective unlabeled homologues occurred in epithelial tissue P4(B) subfractions; this binding was not reversible. Binding specificity was further observed by the competition of 14C-labeled sucrose, fructose and glucose with each unlabeled sugar for binding sites on P4(B) taste bud subfractions; unlabeled sucrose was more effective in competing with each 14C-labeled surgar than was unlabeled fructose or glucose. The relatively non-sweet sugar lactose did not compete with 14C-labeled lactose in P4(B) subfractions from either taste bud or non-taste bud-bearing epithelial tissue. Binding of 14C-labeled sucrose in purified P4(B) bud subfractions was inhibited by increased concentrations of unlabeled sucrose, phospholipase C, neuraminidase, EDTA, NaCl and urea. Dissociation constants for sugar or synthetic sweetener binding were low (approx. 10(-3) M) but in a rank order (sucrose greater than fructose greater than glucose greater than saccharine) consistent with preference and electrophysiological responses in cow. The cow is behaviorally indifferent to saccharine and lactose consistent with the data obtained in the present study.

Animals↗
PubMed1990

Taste-responsive neurons and their locations in the solitary nucleus of the hamster.

The solitary nucleus (nucleus tractus solitarii), the first central relay for taste in mammals, was studied anatomically and physiologically in the golden hamster (Mesocricetus auratus). Activity of neurons to anterior tongue stimulation with sucrose, NaCl and KCl were extracellularly recorded. Electrolytic lesions or horseradish peroxidase deposits allowed subsequent localization of recording sites. Anterior tongue taste-responsive sites were restricted to a very small part of the rostral pole of the solitary nucleus, which is about 3% of the entire nucleus. Sites were confined to the rostral-central and rostral-lateral subdivisions of Whitehead, which contain a number of morphological cell types. Some chemotopic organization was seen with multi-unit recordings, with NaCl-selective sites concentrated rostrally and sucrose- and KCl-selective sites concentrated caudally. Sites with broad sensitivity were distributed throughout the gustatory region. Single neural units showing inhibition to taste stimuli, units highly reactive to all three stimuli, and units with high spontaneous rates were seen in the solitary nucleus, as well as units that responded very selectively and had low spontaneous rates. Single units with similar response profiles to sucrose, NaCl and KCl were not segregated to separate restricted locations within the taste-reactive region; their distributions overlapped. In the hamster, neurons in the anterior tongue taste region of the solitary nucleus process taste quality information in diverse ways. Highly reactive non-specific neurons, neurons that show inhibition, and neurons with high spontaneous rates are more frequently observed in the solitary nucleus than in the afferent input fibers of the chorda tympani nerve. The small region of the rostral pole enclosing taste-responsive neurons is complexly organized in relation to taste quality and contains a number of morphological cell types whose functional role in taste is not yet known.

Action Potentials↗
PubMed2004

Taste perception and coding in Drosophila.

BACKGROUND: Discrimination between edible and contaminated foods is crucial for the survival of animals. In Drosophila, a family of gustatory receptors (GRs) expressed in taste neurons is thought to mediate the recognition of sugars and bitter compounds, thereby controlling feeding behavior. RESULTS: We have characterized in detail the expression of eight Gr genes in the labial palps, the fly's main taste organ. These genes fall into two distinct groups: seven of them, including Gr66a, are expressed in 22 or fewer taste neurons in each labial palp. Additional experiments show that many of these genes are coexpressed in partially overlapping sets of neurons. In contrast, Gr5a, which encodes a receptor for trehalose, is expressed in a distinct and larger set of taste neurons associated with most chemosensory sensilla, including taste pegs. Mapping the axonal targets of cells expressing Gr66a and Gr5a reveals distinct projection patterns for these two groups of neurons in the brain. Moreover, tetanus toxin-mediated inactivation of Gr66a- or Gr5a-expressing cells shows that these two sets of neurons mediate distinct taste modalities-the perception of bitter (caffeine) and sweet (trehalose) taste, respectively. CONCLUSION: Discrimination between two taste modalities-sweet and bitter-requires specific sets of gustatory receptor neurons that express different Gr genes. Unlike the Drosophila olfactory system, where each neuron expresses a single olfactory receptor gene, taste neurons can express multiple receptors and do so in a complex Gr gene code that is unique for small sets of neurons.

Animals↗
PubMed2006

Cortical representation of taste-modifying action of miracle fruit in humans.

Red berries of a tropical plant called miracle fruit, Richadella dulcifica, reduce the sour and aversive taste of acids and add sweet and palatable taste. To elucidate the brain mechanism of this unique action of miracle fruit, we recorded taste-elicited magnetic fields of the human cerebral cortex. The initial taste responses were localized in the fronto-parietal opercular/insular cortex reported as the primary taste area. The mean latency of the response to citric acid after chewing miracle fruit was essentially the same as that for sucrose and was 250-300 ms longer than that for citric acid. Since it is known that stimulation with acids after the action of miracle fruit induces both sweetness and sourness responses in the primate taste nerves, the present results suggest that the sourness component of citric acid is greatly diminished at the level of subcortical relays, and mostly sweetness information reaches the cortical primary taste area. We propose the idea that the qualitative aspect of taste is processed in the primary taste area and the affective aspect is represented by the pattern of activation among the different cortical areas.

Adult↗
PubMed2002

Cooling lesions of the lateral parabrachial nucleus during LiCl activation block acquisition of conditioned taste avoidance in male rats.

Lesions of the lateral parabrachial nucleus (lPBN) disrupt acquisition of LiCl-induced conditioned taste avoidance. Animals with lesions in this area also fail to exhibit taste neophobia. This raises the possibility that an inability of rats to recognize the taste solution as novel contributes to the deficit in taste avoidance learning. If this is the case, then one would expect conditioned taste avoidance not to be disrupted if the lPBN is functional during taste processing but not during LiCl processing. The first three experiments demonstrated that cooling was a viable method by which to temporarily inactivate the lPBN. Measurement of neural temperature during cooling indicated that the lPBN was cooled to temperatures that have been shown to block synaptic transmission but not axonal transmission. Cooling the lPBN itself induced a conditioned avoidance to a sucrose solution but this avoidance was abolished by exposure to daily cooling for 1 week prior to acquisition. In experiment 4, all animals were preexposed to lPBN cooling for 1 week. Those rats that received cooling lesions during a period that started immediately after sucrose solution consumption and extended through the peak effectiveness of LiCl failed to acquire a taste avoidance. These results fail to support the hypothesis that the deficit in taste avoidance learning after permanent lesions of the lPBN is due to an inability of lesioned animals to recognize the taste as novel. They are consistent with the hypothesis that this neural area processes ascending information about LiCl.

Animals↗
PubMed1998

Antagonism between the suppressive effects of NH3 and CO2 on bullfrog taste nerve responses to quinine.

The suppression mechanism of NH3 and CO2 on bullfrog taste nerve responses to 0.1 mM quinine was investigated by applying them directly on the tongue surface (surface application) or at the tongue interstices through the lingual artery (interstitial application). The surface application of NH3 and CO2 reversibly suppressed the taste nerve responses with IC50 values of 0.37 mM and 2.2 mM, respectively, whereas their hydrates were ineffective. The interstitial application of NH3 reversibly suppressed the taste nerve responses. The surface application of CO2 recovered the suppressed responses to quinine. The 4 s application of CO2 prior to that of 0.1 mM quinine had the maximum effect. These results show that NH3-induced alkalosis and CO2-induced acidosis of taste cells, taste nerve endings, or tongue interstices surrounding them suppressed the taste nerve responses, and that the neutralization of their intracellular pH recovered these responses. The time-dependent recovery suggests that the neutralization at a layer inside taste cells, taste nerve endings, or the interstices surrounding them is critical in taste transduction.

Ammonia↗
PubMedDate not supplied

Genetic variation and inferences about perceived taste intensity in mice and men.

The study of genetic variation in taste produces parallels between mice and men. In mice, genetic variation across strains has been documented with psychophysical and anatomical measures as well as with recordings from whole nerves. In humans, the variation has been documented with psychophysical and anatomical measures. Whole-nerve recordings from animals and psychophysical ratings of perceived intensities from human subjects have a similar logical limitation: absolute comparisons across individuals require a standard stimulus that can be assumed equally intense to all. Comparisons across whole-nerve recordings are aided by single-fiber recordings. Comparisons across psychophysical ratings of perceived intensity have been aided by recent advances in methodology; these advances now reveal that the magnitude of genetic variation in human subjects is larger than previously suspected. In females, hormones further contribute to variation in taste. There is evidence that the ability to taste (particularly bitter) cycles with hormones in women of child-bearing age, rises to a maximum early in pregnancy and declines after menopause. Taste affects food preferences, which in turn affect dietary behavior and thus disease risks. Valid assessment of taste variation now permits measurement of the impact of taste variation on health. Advances in psychophysical methodology were essential to understanding genetic variation in taste. In turn, the association of perceived taste intensities with tongue anatomy now provides a new tool for psychophysics. The ability of a psychophysical scale to provide across-subject comparisons can be assessed through its ability to show the fungiform papillae density-taste association.

Animals↗
PubMed2000

Bitter taste perception and severe vomiting in pregnancy.

Hyperemesis gravidarum or severe vomiting during pregnancy is a condition of elusive etiology that can harm both mother and fetus. This study examined the association between increased bitter-taste perception and history of hyperemesis gravidarum. Bitter-taste perception varies genetically and can be altered with conditions that damage taste-related cranial nerves. Sixty women were divided into high- (n = 21) and low-vomit (n = 39) groups based on vomiting exposure across all pregnancies and were screened for genetic variation in taste with bitterness of saturated 6-n-propylthiouracil (PROP) delivered on filter paper. Supertasters perceive PROP as intensely bitter; nontasters, as only weakly. Each reported their history of dysgeusia (persistent taste) and taste-related pathology (otitis media and head trauma). The vomit groups did not differ in the frequency of supertasters, but the high-vomit group had fewest nontasters. The high-vomit group also reported dysgeusia most frequently. A subsample (13 high-vomit and 18 low-vomit women) rated the taste intensity of sodium chloride (1 mol), sucrose (1 mol), citric acid (0.0032 mol), and quinine hydrochloride (0.001 mol) applied to areas innervated by cranial nerves VII and IX. The groups only varied significantly in bitterness of quinine hydrochloride. High-vomit women tasted least bitterness on the anterior tongue (chorda tympani branch of VII) and highest bitterness on the posterior tongue (cranial nerve IX) and palate (superficial petrosal branch of VII). In high-vomit women, elevated bitterness on the posterior tongue and palate does not appear related to hydrochloric acid exposure in vomitus; it may explain the occurrence of dysgeusia. This pattern of spatial taste perception may indicate altered oral sensations that if present during pregnancy, could increase the risk of hyperemesis.

Adult↗
PubMed2003

Differential changes in taste perception induced by benzoic acid prickling.

Benzoic acid (Bz) is a prickling compound used to preserve foods. However, its effects on taste are unknown. This work examines Bz-taste interaction using psychophysical methods [magnitude estimation (ME) and paired comparison (PC)] to measure taste intensity in aqueous solutions of pure tastants (T) and their respective mixtures with 10 mM Bz (Mix). Prototypical tastants induced basic taste qualities (mM): sucrose [90-1440, sweetness (Sw)], citric acid [1-64, sourness (So)], NaCl [15-960, saltiness (Sa)], quinine [0.01-0.64, bitterness (Bitt)], KCl (12.5-400, Sa and Bitt). MEs were analysed using Steven's and Beidler's equations. Bz increased Sw (all concentrations) and ionic tastes (low concentrations) and Bz effects were reduced by concentration increase according with quality and tastant Bz reduced Bitt(Quinine) (high concentrations). Bz reduced taste slopes (percentage decrease): Sw 45% (P<.02), So 34% (P<.01), Sa 35% or 41% (NaCl or KCl, P<.03), Bitt 33% or 60% (quinine P<.01 or KCl P<.04). Bz reduced K(diss) (affinity(-1)) (percentage reduction): Sw 79% (P<.0002), So 40% (P<.03), Sa(NaCl) 63% (P<.005), Sa(KCl) 48% (P<.04), Bitt(KCl) 64% (P<.04). Bz reduced ME(max) (percentage reduction): Sw 31% (P<.004), Bitt(Quinine) 29% (P<.03). PCs confirmed taste increases by Bz (percentage of 'Mix(intensity)>T(intensity)' answers/total answers): Sw 79-69% (90-1440 mM sucrose), So 75% (1 mM citric acid) and 71% (2 mM citric acid), Sa 75-71% (15-120 mM NaCl). Negative concentration dependence of taste increases by Bz suggests different levels of interaction. Biophysical and neurophysiological changes are discussed in relation with Bz properties and mechanism of interaction with taste.

Adult↗
PubMed1997

Relative importance of odour and taste in the one-trial passive avoidance learning bead task.

The relative importance of taste and odour cues in a one-trial passive avoidance learning (PAL) task was examined. One-day-old chicks were presented with a small bead and different combinations of the taste and odour of methyl anthranilate (MeA). The chicks had received three consecutive pretraining trials where they were presented with white, red, and blue beads. They were then trained with a red bead presented in one of four possible conditions: dry and unscented, with the odour but not the taste of MeA, with the bitter taste but not the odour of MeA (the chicks' nostrils were occluded with a wax preparation), or with the taste and odour of MeA. Recall was tested 10 min after training by presenting a red and then a blue bead with no odour or taste added. The number of pecks made at the bead and the number of bouts of head shaking during each of the trials were scored. During testing, chicks that were trained with the odour of MeA alone pecked less at a red bead than at a blue bead, compared with chicks trained with a dry and unscented bead, indicating that they discriminated between the training bead and a bead of a different colour. There was no significant difference between the discrimination ratio of chicks trained with the odour, taste, or taste and odour of MeA. These results demonstrate that chicks can perform PAL using taste and/or odour cues.

Animals↗
PubMedDate not supplied

Making sense with TRP channels: store-operated calcium entry and the ion channel Trpm5 in taste receptor cells.

The sense of taste plays a critical role in the life and nutritional status of organisms. During the last decade, several molecules involved in taste detection and transduction have been identified, providing a better understanding of the molecular physiology of taste receptor cells. However, a comprehensive catalogue of the taste receptor cell signaling machinery is still unavailable. We have recently described the occurrence of calcium signaling mechanisms in taste receptor cells via apparent store-operated channels and identified Trpm5, a novel candidate taste transduction element belonging to the mammalian family of transient receptor potential channels. Trpm5 is expressed in a tissue-restricted manner, with high levels in gustatory tissue. In taste cells, Trpm5 is co-expressed with taste-signaling molecules such as alpha-gustducin, Ggamma(13), phospholipase C beta(2) and inositol 1,4,5-trisphosphate receptor type III. Biophysical studies of Trpm5 heterologously expressed in Xenopus oocytes and mammalian CHO-K1 cells indicate that it functions as a store-operated channel that mediates capacitative calcium entry. The role of store-operated channels and Trpm5 in capacitative calcium entry in taste receptor cells in response to bitter compounds is discussed.

Animals↗