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PubMed1998

The morphogenesis of mouse vallate gustatory epithelium and taste buds requires BDNF-dependent taste neurons.

The developmental absence of brain-derived neurotrophic factor (BDNF) in null mutant mice caused three interrelated defects in the vallate gustatory papilla: sparse innervation, a reduction in the area of the gustatory epithelium, and fewer taste buds. On postnatal day 7, the stunted vallate papilla of bdnf null mutant mice was 30% narrower, the trench walls 35% reduced in area, and the taste buds 75% less abundant compared with wild-type controls. Quantitative assessment of innervation density was carried out to determine if the small trench walls and shortage of taste buds could be secondary consequences of the depletion of gustatory neurons. The diminished gustatory innervation was linearly associated with a reduced trench wall area (r = +0.94) and fewer taste buds (r = +0.96). Residual taste buds were smaller than normal and were innervated by a few surviving taste neurons. We conclude that BDNF-dependent taste neurons contribute to the morphogenesis of lingual gustatory epithelia and are necessary for both prenatal and postnatal mammalian taste bud formation. The gustatory system provides a conspicuous example of impaired sense organ morphogenesis that is secondary to sensory neuron depletion by neurotrophin gene null mutation.

Animals↗

PubMed1985

Ultrastructure of mouse vallate taste buds. I. Taste cells and their associated synapses.

The ultrastructural features of murine vallate taste bud cells and their associated synapses have been examined in thin and thick sections with conventional transmission electron microscopy and high-voltage electron microscopy. Computer-assisted reconstructions from serial sections were utilized to aid in visualization of taste bud cell-nerve fiber synapses. We have classified taste bud cells on the basis of previously established criteria-namely, size of the nucleus, shape and density of chromatin, density of cytoplasm, and presence or absence of dense-cored or clear vesicles, other cytoplasmic organelles, and synaptic foci. Both dark cells and light cells are present, as well as cells with intermediate morphological characteristics. Synapses were observed from taste bud cells onto nerve fiber processes. In virtually all instances, synapses are associated with the nuclear region of the taste cell. These synapses are characterized by the presence of 40-70 nm clear vesicles embedded in a thickened presynaptic membrane separated from the postsynaptic membrane by a 16-30 nm cleft. Synapses are not unique to any particular cell type. Dark, intermediate, and light cells all synapse onto nerve fibers. Two general types of synapses exist: spot (or macular) and fingerlike. In the latter, the postsynaptic region of the neuronal process protrudes into an invagination of the taste cell membrane. Differences in synaptic morphology are not correlated with taste cell type. In some cases a single taste cell was observed to possess both macular and fingerlike synapses adjacent to one another, forming a synaptic complex onto a single neuronal process. On the basis of the presence of synaptic contacts, we conclude that both "dark" and "light" cells are gustatory receptors.

Animals↗

PubMed1995

NMDA and non-NMDA receptors mediate taste afferent inputs to cortical taste neurons in rats.

Two main subclasses of ionotropic receptors for excitatory amino acids (EAAs), N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors, are involved in neurotransmission in the cortex of mammals. To examine whether EAAs are transmitters at the cortical taste area (CTA) in rats and to elucidate which types of the two ionotropic receptors operate at these synapses, we studied the effects of microiontophoretic administration of EAA antagonists on the responses of 64 taste cortical neurons to four basic taste stimuli in urethane-anesthetized rats. Both D-2-amino-5-phosphonovalerate (APV), a selective antagonist for NMDA receptors, and 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), a selective antagonist for non-NMDA receptors, suppressed most of the taste responses. The percentage of neurons suppressed by APV (70.3%) was almost the same as that suppressed by CNQX (64.1%). These suppressive effects were independent of the effects of background discharges during the prestimulus, water-rinsing period. The percentage of neurons suppressed by the antagonists did not differ between any pairs of taste stimuli. The number of neurons possessing both receptors was larger in the granular insular area (area GI), one of the two CTAs, than in the dysgranular insular area (area DI). In addition, taste responses were suppressed by CNQX or by both APV and CNQX in area GI in a significantly larger number of layer V neurons than in area DI. The present results indicate that normal excitatory transmission of taste afferents in the CTA in rats was mediated by both NMDA and non-NMDA receptors. The finding that a large fraction of neurons in the CTA in rats mediated taste information through NMDA receptors in normal transmission might be related to the higher potency of the plasticity observed in the CTA.

2-Amino-5-phosphonovalerate↗

PubMed1989

Conditioned taste preference produced by pairing a taste with a low dose of morphine or sufentanil.

Taste conditioning produced by pairing a taste with low doses of morphine or sufentanil was studied in rats in five experiments. Conditioned taste preferences were obtained with a trace conditioning procedure in which ingestion of a flavored solution was followed by an injection of sufentanil, either 0.25 mcg/kg in experiment 1 or 0.50 mcg/kg in experiment 2. Morphine produced less consistent results than sufentanil. When a similar trace conditioning procedure was used with morphine, a dose of 0.25 mg/kg produced no observable taste conditioning in experiment 3 while 0.42 mg/kg was marginally effective in producing a conditioned taste aversion in experiment 4. In experiment 5, however, conditioning of a taste preference was produced by 0.42 mg/kg morphine with a simultaneous conditioning procedure in which the morphine injection preceded ingestion of the flavored solution. The simultaneous procedure was presumed to facilitate the conditioning of taste preference by minimizing the conditioning of taste aversion.

Analgesics↗

PubMed1994

Morphine-conditioned analgesia using a taste cue: dissociation of taste aversion and analgesia.

The present study examined the ability of a taste cue to serve as a conditioned stimulus (CS) for conditioning the analgesic effect of morphine. Rats were given three pairings of a taste CS with a morphine unconditioned stimulus (US). As expected, there was a decrease in CS intake across repeated pairings, indicating that a conditioned taste aversion was obtained. More important, presentation of the CS alone also increased paw-lick latencies on a hot plate test (either 50 degrees C or 54 degrees C hot plate), suggesting that an analgesic conditioned response (CR) was obtained. The dose of morphine required to produce conditioned analgesia was higher than the dose of morphine required to produce conditioned taste aversion. Using 15 mg/kg morphine, however, both conditioned taste aversion and conditioned analgesia were present when the morphine US was given immediately following CS intake, but not when given 6 h following CS intake. In contrast to morphine, pairing a taste CS with lithium produced a conditioned taste aversion without any conditioned analgesic response. These results indicate that acquisition of an analgesic CR is not the result of stress induced by an aversion to the taste CS.

Analgesia↗

PubMed1987

Interactions between radiation and amphetamine in taste aversion learning and the role of the area postrema in amphetamine-induced conditioned taste aversions.

Three experiments were run to assess the role of the area postrema in taste aversion learning resulting from combined treatment with subthreshold unconditioned stimuli and in the acquisition of an amphetamine-induced taste aversion. In the first experiment, it was shown that combined treatment with subthreshold radiation (15 rad) and subthreshold amphetamine (0.5 mg/kg, IP) resulted in the acquisition of a taste aversion. The second experiment showed that lesions of the area postrema blocked taste aversion learning produced by two subthreshold doses of amphetamine. In the third experiment, which looked at the dose-response curve for amphetamine-induced taste aversion learning in intact rats and rats with area postrema lesions, it was shown that both groups of rats acquired taste aversions following injection of amphetamine, although the rats with lesions showed a less severe aversion than the intact rats. The results are interpreted as indicating that amphetamine-induced taste aversion learning may involve area postrema-mediated mechanisms, particularly at the lower doses, but that an intact area postrema is not a necessary condition for the acquisition of an amphetamine-induced taste aversion.

Amifostine↗

PubMed2006

Differential taste coding of salt and acid by correlative activities between taste-sensitive neuron types in rat gustatory cortex.

Using a multi-electrode recording technique, the present study aimed to elucidate the role of broadly-tuned taste-sensitive neurons in the rat gustatory cortex in discriminating between salt and acid. A majority of taste-sensitive neurons (94/119 neurons; 78%) were classified as NaCl (N)-, HCl (H)- or NaCl and HCl (NH)-best neurons. Of 63 neuron pairs (94 neurons), 31 showed significant peaks and/or troughs in their cross-correlograms (CCs) during taste stimulation periods. During NaCl stimulation, the incidence of significant correlation and the mean frequency of correlated discharges (FC) in the N/N and NH/NH pairs were higher than those in the other best-taste pairs. In contrast, during HCl stimulation both indices in the N/N or H/H pairs were very low, while those in the NH/NH pairs were high. These results suggest that (1) correlated activities between N-best neurons and those between NH-best neurons play a significant role in taste quality coding of salt, and that (2) correlated activities between NH-best neurons may be important for sour taste coding as well. Peak formation in CCs tended to be more frequent in the homo-types (N/N, H/H and NH/NH pairs) than in the hetero-types (N/NH, N/H and H/NH pairs). In contrast, troughs were observed mostly in the hetero-types. Inhibitory interaction in hetero-type pairs together with coactivation in homo-type pairs may enhance taste discrimination by taste-sensitive neuron populations.

Algorithms↗

PubMed2006

Effect of previous taste experiences on taste neophobia in young-adult and aged rats.

Neophobia is an innate response that can be defined as the reluctance to consume novel-tasting substances. The differential effect of previous aversive and nonaversive taste memory on a subsequent neophobic response was studied in young-adult (Experiment 1) and aged rats (Experiment 2). Surprising, a previous nonaversive taste experience eliminated the subsequent neophobic response to a solution of 1% sodium chloride (NaCl) in young-adult and aged rats. This result is interpreted as a generalization of the previous safe taste memory and the emotional responses that might be induced when a new taste is presented. However, a differential effect associated with aging was found for a previous aversive taste memory induced with a low dose of lithium chloride (0.15 M; 1% b.w.). While in young-adult rats this aversive taste memory did not change the neophobic response to an NaCl solution, in aged rats this memory potentiated the subsequent neophobic response to NaCl. This result is interpreted as an increase in the generalization of aversive taste memory and the emotional responses associated with aging.

Aging↗

PubMed1998

Intracellular free calcium concentration in human taste bud cells increases in response to taste stimuli.

We examined changes of intracellular free calcium concentration [Ca2+]i elicited by taste stimuli of sucrose, denatonium and NaCl in the taste buds of seven human fungiform papillae. In one taste bud we observed an increase in [Ca2+]i induced by only NaCl. In another bud an increase of [Ca2+]i in response to both NaCl and sucrose was found. The Ca2+ responses to NaCl and sucrose occurred in differential areas within the one taste bud. In the other five fungiform papillae [Ca2+]i was not changed by the taste stimuli. These results suggest that an increase of [Ca2+]i participates in taste transduction mechanisms for sucrose and NaCl, and that taste cells in one taste bud may respond to differential stimuli.

Adult↗

PubMed2004

Odor of taste stimuli in conditioned "taste" aversion learning.

The present research addresses whether rats can express odor aversions to the odor of taste stimuli. In Experiment 1, saccharin or salt were either mixed in distilled water, so the rats could taste and smell them, or presented on disks attached to the tubes' metal spouts so the rats could only smell them. Aversions were established to taste stimuli under both conditions. The results of Experiment 2 indicate that conditioning was to the odor of the tastes when they were presented on disks in Experiment 1, hence both taste and odor aversions were established by means of "taste" stimuli. Taste aversion learning thus may more properly be termed flavor aversion learning, with flavor referring to both taste and odor components.

Animals↗

PubMed1988

Apical localization of K+ channels in taste cells provides the basis for sour taste transduction.

Previous studies have shown that mudpuppy taste receptor cells respond to sour taste stimuli (weak acids) with depolarizing receptor potentials or action potentials that are blocked by the K+ channel blocker tetraethylammonium. Voltage-clamp recordings from isolated taste cells indicated that taste receptor cells exhibit a variety of voltage-dependent conductances and that acids reduce a voltage-dependent K+ current. Since taste stimuli are restricted to the apical surface of the intact tongue, only 1-2% of the taste receptor cell surface is exposed to chemical stimuli. Thus, modification of a K+ conductance would be an effective transduction mechanism in receptor cells only if the majority of K+ channels were located on the apical membrane. We have used a combination of "loose-patch" and whole-cell recording methods to map the distribution of voltage-sensitive K+ and Na+ channels on dissociated Necturus maculosus taste cells. We report here that the K+ conductance is approximately equal to 50-fold greater on apical membrane than on basolateral membrane, whereas the Na+ conductance is distributed evenly. The marked nonuniformity of the voltage-sensitive K+ conductance, together with the block of this conductance by sour stimuli, indicates that K+ current modulation is the mechanism of sour taste transduction.

Animals↗

PubMed2001

IP(3) receptor type 3 and PLCbeta2 are co-expressed with taste receptors T1R and T2R in rat taste bud cells.

The Ca(2+) signaling cascade has been reported to be activated by many tastants in vertebrate taste systems. Recently we have shown that G(i2) and phospholipase Cbeta2 (PLCbeta2) are co-expressed in a subset of taste bud cells and are possibly involved in Ca(2+) triggering of taste signaling in rats. We report here that, as a component downstream of PLCbeta2, the type 3 isoform of the inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R3) is specifically expressed in the same cells as PLCbeta2 in rat taste buds. We also show that cells expressing rT2R9, a probable cycloheximide receptor, are included among PLCbeta2- and IP(3)R3-positive cells, as in the case of rT1R2, a different type of taste receptor. Our findings indicate that PLCbeta2 and IP(3)R3 co-localize together with G(i2) as downstream components of two different types of taste receptors, T1R and T2R, in taste bud cells.

Animals↗

PubMed1998

The morphogenesis of mouse vallate gustatory epithelium and taste buds requires BDNF-dependent taste neurons

The developmental absence of brain-derived neurotrophic factor (BDNF) in null mutant mice caused three interrelated defects in the vallate gustatory papilla: sparse innervation, a reduction in the area of the gustatory epithelium, and fewer taste buds. On postnatal day 7, the stunted vallate papilla of bdnf null mutant mice was 30% narrower, the trench walls 35% reduced in area, and the taste buds 75% less abundant compared with wild-type controls. Quantitative assessment of innervation density was carried out to determine if the small trench walls and shortage of taste buds could be secondary consequences of the depletion of gustatory neurons. The diminished gustatory innervation was linearly associated with a reduced trench wall area (r=+0.94) and fewer taste buds (r=+0.96). Residual taste buds were smaller than normal and were innervated by a few surviving taste neurons. We conclude that BDNF-dependent taste neurons contribute to the morphogenesis of lingual gustatory epithelia and are necessary for both prenatal and postnatal mammalian taste bud formation. The gustatory system provides a conspicuous example of impaired sense organ morphogenesis that is secondary to sensory neuron depletion by neurotrophin gene null mutation.

Journal Article↗

PubMed1976

Biochemical studies of taste sensation: II. Labelling of cyclic AMP of bovine taste papillae in response to sweet and bitter stimuli.

Labeling of cyclic AMP of tase papillae and its responsiveness to tast stimuli has been measured using whole papillae from bovine tongue prelabeled with [ 8-(14) C] adenine. Labeling was measured in circumvallate and fungiform papillae, both of which contain taste buds, and in filiform papillae and small blocks of tongue epithelium, which are devoid of taste buds. No differences were observed in the levels of activity. The labeling of cyclic AMP of circumvallate papillae showed only small increases (12-22%) in the presence of the taste stimulus sucrose (sweet), and the stimulatory effects were not statistically significant. The increase due to sucrose was not potentiated by theophylline. No stimulation by sucrose was observed with epithelium controls. Lactose, which is a poor taste stimulus, did not stimulate labeling of cyclic AMP in taste papillae. Theophylline, caffeine, and quinine (bitter) stimulated labeling of cyclic AMP by up to 2-fold, as did L-Epinephrine. Evidence for a specific role of cyclic AMP as a second messenger in taste sensation was not obtained. It is suggested that cyclic AMP might provide a mechanistic basis for studying some of the effects of sweet and bitter compounds in mixtures.

Adenine↗

PubMed2006

Altering expectancy dampens neural response to aversive taste in primary taste cortex.

The primary taste cortex consists of the insula and operculum. Previous work has indicated that neurons in the primary taste cortex respond solely to sensory input from taste receptors and lingual somatosensory receptors. Using functional magnetic resonance imaging, we show here that expectancy modulates these neural responses in humans. When subjects were led to believe that a highly aversive bitter taste would be less distasteful than it actually was, they reported it to be less aversive than when they had accurate information about the taste and, moreover, the primary taste cortex was less strongly activated. In addition, the activation of the right insula and operculum tracked online ratings of the aversiveness for each taste. Such expectancy-driven modulation of primary sensory cortex may affect perceptions of external events.

Adolescent↗

PubMed2001

Decrease in rat taste receptor cell intracellular pH is the proximate stimulus in sour taste transduction.

Taste receptor cells (TRCs) respond to acid stimulation, initiating perception of sour taste. Paradoxically, the pH of weak acidic stimuli correlates poorly with the perception of their sourness. A fundamental issue surrounding sour taste reception is the identity of the sour stimulus. We tested the hypothesis that acids induce sour taste perception by penetrating plasma membranes as H(+) ions or as undissociated molecules and decreasing the intracellular pH (pH(i)) of TRCs. Our data suggest that taste nerve responses to weak acids (acetic acid and CO(2)) are independent of stimulus pH but strongly correlate with the intracellular acidification of polarized TRCs. Taste nerve responses to CO(2) were voltage sensitive and were blocked with MK-417, a specific blocker of carbonic anhydrase. Strong acids (HCl) decrease pH(i) in a subset of TRCs that contain a pathway for H(+) entry. Both the apical membrane and the paracellular shunt pathway restrict H(+) entry such that a large decrease in apical pH is translated into a relatively small change in TRC pH(i) within the physiological range. We conclude that a decrease in TRC pH(i) is the proximate stimulus in rat sour taste transduction.

Acetic Acid↗

PubMed1997

Tastes activate different second messengers in taste cells.

Taste signal transduction occurs in the microvillous membrane of taste cells. Previously, we hypothesized that c-GMP may mediate sweet taste transduction. Some data indicated that IP3 may have a role in vertebrate bitter taste transduction. Here we report that the different second messengers are activated by different tastes. We used techniques designed for radioimmunoassay measurement. The results indicate that sucrose triggers an increase in c-GMP concentration and quinine increases the IP3 concentration in mouse taste cells. These results support the sweet and bitter taste transduction hypotheses.

Animals↗

PubMed1977

Taste acuity of the human palate. I. Studies with electrogustometry and taste solutions on young adults.

The purposes of the study were to determine whether or not taste perception was present in the area which would have been covered by the base plate of a full upper denture and, if taste perception was present there, to compare its strength to that of the remainder of the soft palate and of the apex and base of the tongue. The taste acuity of 32 dental students was measured at the apex and base of the tongue and on the hard and soft palate using two methods, an electric current and sweet, salty, sour and bitter test solutions, the latter in order to determine whether or not there exist differences in the perception of the different taste modalities in these areas. No taste perception could be demonstrated on the hard palate except in the region close to the border between the hard and soft palate, where the threshold values were very high compared with those for the soft palate immediately behind this border and for the tongue. The inter-individual range of the threshold values for the soft palate was very large. Further studies on the taste acuity of the human palate and its role in the total perception of taste are indicated.

Adult↗