Rat Taste Research Articles

Modeling and simulation of ion channels and action potentials in taste receptor cells

Based on patch clamp data on the ionic currents of rat taste receptor cells, a mathematical model of mammalian taste receptor cells was constructed to simulate the action potentials of taste receptor cells and their corresponding ionic components, including voltage-gated Na(+) currents and outward delayed rectifier K(+) currents. Our simulations reproduced the action potentials of taste receptor cells in response to electrical stimuli or sour tastants. The kinetics of ion channels and their roles in action potentials of taste receptor cells were also analyzed. Our prototype model of single taste receptor cell and simulation results presented in this paper provide the basis for the further study of taste information processing in the gustatory system.

Effects of sodium depletion on detection thresholds for salty taste in rats

Previous studies, which have mostly focused on concentrated NaCl solution intake, have suggested sodium depletion may be accompanied with salt taste sensory changes. To further investigate whether the function of the salt taste system changes in different patterns for highly concentrated and diluted NaCl taste stimuli, the effects of sodium depletion on NaCl taste detection threshold in rats were examined. After a conditioned taste aversion (CTA) to a suprathreshold concentration of NaCl (0.1 M) was established, rats were given a series of two-bottle choice tests between distilled water and different concentrations of NaCl. Conditioned rats will generalize the aversion to diluted solutions when they are detected. The taste detection threshold for NaCl is defined as the lowest concentration at which there is a reliable difference in the preference scores between conditioned and control subjects. The results showed that detection threshold for NaCl lay between 0.003 M and 0.005 M in sodium-replete rats, whereas in sodium-depleted rats that have an amplified action of angiotensin II in the brain, the threshold significantly decreased to be between 0.0001 M and 0.0003 M. However, in rats with a blocked action of angiotensin II in the brain the decreased NaCl detection threshold was between 0.001 M and 0.003 M. These findings suggest that sodium-depleted rats could decrease the NaCl taste detection threshold to increase the ability to find sodium ions. And the regulation of the salt taste sensitivity may be related to the action of angiotensin II in brain.

Effects of dietary Na+ deprivation on epithelial Na+ channel (ENaC), BDNF, and TrkB mRNA expression in the rat tongue

BackgroundIn rodents, dietary Na+ deprivation reduces gustatory responses of primary taste fibers and central taste neurons to lingual Na+ stimulation. However, in the rat taste bud cells Na+ deprivation increases the number of amiloride sensitive epithelial Na+ channels (ENaC), which are considered as the "receptor" of the Na+ component of salt taste. To explore the mechanisms, the expression of the three ENaC subunits (α, β and γ) in taste buds were observed from rats fed with diets containing either 0.03% (Na+ deprivation) or 1% (control) NaCl for 15 days, by using in situ hybridization and real-time quantitative RT-PCR (qRT-PCR). Since BDNF/TrkB signaling is involved in the neural innervation of taste buds, the effects of Na+ deprivation on BDNF and its receptor TrkB expression in the rat taste buds were also examined.ResultsIn situ hybridization analysis showed that all three ENaC subunit mRNAs were found in the rat fungiform taste buds and lingual epithelia, but in the vallate and foliate taste buds, only α ENaC mRNA was easily detected, while β and γ ENaC mRNAs were much less than those in the fungiform taste buds. Between control and low Na+ fed animals, the numbers of taste bud cells expressing α, β and γ ENaC subunits were not significantly different in the fungiform, vallate and foliate taste buds, respectively. Similarly, qRT-PCR also indicated that Na+ deprivation had no effect on any ENaC subunit expression in the three types of taste buds. However, Na+ deprivation reduced BDNF mRNA expression by 50% in the fungiform taste buds, but not in the vallate and foliate taste buds. The expression of TrkB was not different between control and Na+ deprived rats, irrespective of the taste papillae type.ConclusionThe findings demonstrate that dietary Na+ deprivation does not change ENaC mRNA expression in rat taste buds, but reduces BDNF mRNA expression in the fungiform taste buds. Given the roles of BDNF in survival of cells and target innervation, our results suggest that dietary Na+ deprivation might lead to a loss of gustatory innervation in the mouse fungiform taste buds.

GABA expression in the mammalian taste bud functions as a route of inhibitory cell-to-cell communication

Recent advances have underscored cell-to-cell communication as an important component of the operation of taste buds with individual taste receptor cells (TRCs) communicating with one another by means of a number of neurotransmitters and neuropeptides, although functional roles are not yet understood. Here, we characterize the presence, distribution pattern, phenotype, and functional consequences of a previously undescribed inhibitory route within the taste bud mediated by the classic neurotransmitter GABA and its receptors. By using immunocytochemistry, subsets of TRCs within rat taste buds were identified as expressing GABA, and its synthetic enzyme glutamate decarboxylase (GAD). GAD expression was verified with Western blotting. Immunofluorescent studies revealed complex coexpression patterns of GAD with the TRC protein markers gustducin, neural cell adhesion molecule, protein gene product 9.5, and synaptosomal-associated protein of 25 kDa that collectively outline hardwired signaling pathways of GABAergic TRCs. RT-PCR and immunocytochemistry demonstrated that both GABA(A) and GABA(B) receptors are expressed in the taste bud. The later was observed in a subset TRCs paracrine to GAD-expressing TRCs. Physiological effects of GABA were examined by patch clamp recordings. GABA and the GABA(A) agonists muscimol and isoguvacine enhanced isolated chloride currents in a dose-dependent manner. Also, GABA and the GABA(B) agonist baclofen both elicited increases of the inwardly rectifying potassium currents that could be blocked by the GABA(B) receptor antagonist CGP 35348 and the G protein blocker GDP-betaS. Collectively, these data suggest that GABAergic TRCs are able to shape the final chemosensory output of the bud by means of processes of cell-to-cell modulation.

Hedonics of taste influence the gastric emptying in rats

It is known that taste sensation plays important roles in various functions including appetite, nutriental choices, food intake and digestion. To study the modulation of digestive functions by taste stimulation, we measured the gastric emptying of experimental foods with appetitive or aversive tastes in Wistar male rats. Rats were randomly divided into 3 groups: each group was trained to eat a mash mixture (8 g) made up with powdered food (4 g) and a solution (4 g) for 30 min per day. The solution was either distilled water, saccharin solution as a palatable taste, or quinine solution as an aversive taste. On the test day, the contents of the stomach of each rat were measured before and 30, 150, or 300 min after the start of eating the mash. The results showed that the food output from the stomach was increased by the palatable mash and was decreased by the aversive mash in comparison with non-adulterated mash 150 min after eating. There were no significant differences in gastric emptying among the 3 groups after deafferentation of the two peripheral taste nerve branches, the chorda tympani and glossopharyngeal nerves, or after intragastric infusions of each mash. After the establishment of conditioned taste aversions to saccharin, saccharin mash became ineffective in increasing gastric emptying. These results show that hedonically positive tastes increase, but hedonically negative tastes decrease gastric function in terms of gastric emptying.

Resynthesis of phosphatidylinositol 4,5‐bisphosphate mediates adaptation of the caffeine response in rat taste receptor cells

Caffeine, a prototypic bitter stimulus, produces several physiological actions on taste receptor cells that include inhibition of KIR and KV potassium currents and elevations of intracellular calcium. These responses display adaptation, i.e. their magnitude diminishes in the sustained presence of the stimulus. Levels of the membrane lipid phosphatidylinositol-4,5-bisphosphate (PIP2) are well known to modulate many potassium channels, activating the channel by stabilizing its open state. Here we investigate a putative relationship of KIR and KV with PIP2 levels hypothesizing that inhibition of these currents by caffeine might be allayed by PIP2 resynthesis. Using standard patch-clamp techniques, recordings of either potassium current from rat posterior taste receptor cells produced essentially parallel results when PIP2 levels were manipulated pharmacologically. Increasing PIP2 levels by blocking phosphoinositide-3 kinase with wortmannin or LY294002, or by blocking phospholipase C with U73122 all significantly increased the incidence of adaptation for both KIR and KV. Conversely, lowering PIP2 synthesis by blocking PI4K or using the PIP2 scavengers polylysine or bovine serum albumin reduced the incidence of adaptation. Adaptation could be modulated by activation of protein kinase C but not calcium calmodulin kinase. Collectively, these data support two highly novel conclusions: potassium currents in taste receptor cells are significantly modulated by PIP2 levels and PIP2 resynthesis may play a central role in the gustatory adaptation process at the primary receptor cell level.

Type II and III Taste Bud Cells Preferentially Expressed Kainate Glutamate Receptors in Rats.

Glutamate-induced cobalt uptake reveals that non-NMDA glutamate receptors (GluRs) are present in rat taste bud cells. Previous studies involving glutamate induced cobalt staining suggest this uptake mainly occurs via kainate type GluRs. It is not known which of the 4 types of taste bud cells express subunits of kainate GluR. Circumvallate and foliate papillae of Sprague-Dawley rats (45~60 days old) were used to search for the mRNAs of subunits of non-NMDA GluRs using RT-PCR with specific primers for GluR1-7, KA1 and KA2. We also performed RT-PCR for GluR5, KA1, PLCbeta2, and NCAM/SNAP 25 in isolated single cells from taste buds. Taste epithelium, including circumvallate or foliate papilla, express mRNAs of GluR5 and KA1. However, non-taste tongue epithelium expresses no subunits of non-NMDA GluRs. Isolated single cell RT-PCR reveals that the mRNAs of GluR5 and KA1 are preferentially expressed in Type II and Type III cells over Type I cells.

Taste, olfactory and trigeminal neophobia in rats with forebrain lesions

The present study was designed to examine whether lesions of the insular cortex (IC; Experiment 1), the basolateral amygdala (BLA) or medial amygdala (MeA; Experiment 2) influence the neophobic reactions to orally consumed liquid stimuli. Three different types of stimuli were used: taste (0.5% saccharin), olfactory (0.1% amyl acetate), and trigeminal (0.01 mM capsaicin). Rats with IC, BLA and MeA lesions showed normal responses to the olfactory and trigeminal stimuli. Each type of lesion, however, disrupted the initial occurrence of neophobia to the taste stimulus. The significance of these findings to conditioned taste aversion is discussed.

Expression of α-gustducin in the circumvallate papillae of taste buds of diabetic rats

Taste impairment is a complication of Diabetes mellitus and some studies have shown this taste disorder in diabetes. Diabetes can decrease the ability of individuals to detect and recognize sweet, salty and bitter tastes. alpha-Gustducin is a transducin-like G-protein selectively expressed in 20 - 30% of taste receptor cells, which has been shown to be involved in bitter, sweet and umami taste responses. The present study was performed to explore the protein and mRNA expression of alpha-gustducin in the taste buds of diabetic and control rat circumvallate papillae. Our results showed that the positive expression of alpha-gustducin in diabetic rat taste bud cells is higher than that in normal controls as shown by both immunohistochemistry and RT-PCR. There may be some variant of bitter, sweet or umami taste transduction during diabetes and that taste transduction variant may be one cause of diabetic taste impairment.

Behavioral comparison of sucrose and l-2-amino-4-phosphonobutyrate (l-AP4) tastes in rats: Does l-AP4 have a sweet taste?

Even though it is generally thought that umami stimuli such as monosodium glutamate (MSG) and sweet stimuli such as sucrose are detected by different taste receptors, these stimuli appear to share taste qualities when amiloride (a sodium channel blocker) is present to reduce the sodium taste. Single fiber recording studies of the facial and glossopharyngeal nerves have shown that encoding of l-2-amino-4-phosphonobutyrate (l-AP4), a potent mGluR4 agonist that elicits a taste quite similar to MSG, may occur in the same fibers that also encode sweet stimuli. This suggests that l-AP4 and sweet substances may activate common receptors or afferent signaling mechanisms. We report results of behavioral experiments that test this hypothesis. In the first study, rats conditioned to avoid sucrose or l-AP4 generalized the aversion to the opposite substance, indicating that both substances elicited similar tastes. However, two taste discrimination experiments showed that rats easily discriminated between sucrose and l-AP4 over a wide range of concentrations, even when the cue function of sodium associated with l-AP4 was reduced by amiloride and neutralized by adding equimolar concentrations of NaCl to sucrose. These data suggest that even though l-AP4 and sucrose elicit similar taste qualities, one or both substances also elicit other taste qualities not shared by the opposite substance. They also suggest that the taste-mGluR4 receptor and the signal pathway activated by l-AP4 are not the same as those activated by sucrose. These data, when combined with fiber recording data, suggest that there is convergence of l-AP4 and sucrose signals at some point early in the gustatory pathway.

Domperidone interferes with conditioned disgust reactions but not taste avoidance evoked by a LiCl‐paired taste in infant rats

Rats exhibit taste avoidance and conditioned disgust reactions when stimulated with a tastant paired with lithium chloride (LiCl). Lithium-mediated activation of chemoreceptor nuclei at the brainstem appears to determine the acquisition of conditioned taste aversion (CTA) in adult rodents. Domperidone (DOM), an anti-emetic drug that does not cross the blood-brain barrier, was employed to analyze mechanisms underlying LiCl-mediated CTA in infant rats. On postnatal day 13 animals were given DOM followed by a pairing between intraoral saccharin and LiCl. Saccharin consumption at testing was lower in lithium-treated pups than in controls. DOM did not interfere with this LiCl-mediated taste avoidance but significantly decreased LiCl-mediated disgust reactions (head-shaking and wall climbing). Activation of the emetic system of the brainstem does not seem necessary for the acquisition of LiCl-mediated conditioned taste avoidance. Yet, these centers seem to be involved in the palatability shift resulting from taste-LiCl pairings. These results indicate an early dissociation between conditioned disgust reactions and conditioned taste avoidance.

Cytokeratin 14 is expressed in immature cells in rat taste buds

We analyzed the differentiation of taste bud cells, by precisely describing expression profiles of cytokeratins (CKs) 8 and 14 in relation to those of marker molecules including label of 5-bromo-2'-deoxy uridine (BrdU) injected. In rat circumvallate papillae, cell division was observed at the basal layer of the epithelium expressing CK14 and located outside taste buds. The progenitor cells began to migrate toward the apical surface and maintained CK14 expression at 1 day after BrdU injection (day 1). On the other hand, a minor population of newly divided cells was infrequently incorporated into taste buds and also maintained CK14 expression at day 1. In taste buds, the conversion of CK subtypes occurred from CK14 to cytokeratin 8 (CK8) at day 2-3, showing the differentiation from immature cells expressing CK14 into mature or maturing cells expressing CK8. Functionally matured cells such as taste receptor cells expressing inositol triphospate receptor type 3 (IP(3)R3) never expressed CK14, suggesting that CK14 would be expressed only in immature cells. On the other hand, a small but distinct population of BrdU-positive cells still showed CK14 immunoreactivity in taste buds even at day 12, which might correspond to the cells that remain undifferentiated for a long period within taste buds.

Gustducin and transducin: a tale of two G proteins.

In the vertebrate taste cell, heterotrimeric guanine nucleotide-binding proteins (G proteins) are involved in the transduction of both bitter and sweet taste stimulants. The bitter compound denatonium raises the intracellular Ca2+ concentration in rat taste cells, apparently via G protein-mediated increases in inositol trisphosphate. Sucrose causes a G protein-dependent generation of cAMP in rat taste bud membranes; elevation of cAMP levels leads to taste cell depolarization. To identify and characterize those proteins involved in the taste transduction process, we have cloned G protein alpha subunit (G alpha) cDNAs from rat taste cells. Using degenerate primers corresponding to conserved regions of G proteins, we used the polymerase chain reaction to amplify and clone taste cell G alpha cDNAs. Eight distinct G alpha cDNAs were isolated, cloned and sequenced from a taste cell library. Among these clones was alpha gustducin, a novel taste G alpha closely related to the transducins. In addition to alpha gustducin, we cloned rod and cone transducins from taste cells. This is the first identification of transducin expression outside photoreceptor cells. The primary sequence of alpha gustducin shows similarities to the transducins in the receptor interaction domain and the phosphodiesterase activation site. These sequence similarities suggest that gustducin and transducin regulate taste cell phosphodiesterase, probably in bitter taste transduction.

Comparison of l-monosodium glutamate and l-amino acid taste in rats

T1R2/T1R3 heterodimers are selectively responsive to sweet substances whereas T1R1/T1R3 receptors are selective for umami substances, represented by monosodium glutamate (MSG), and for l-amino acids. If a single receptor is responsible for detection of umami and l-amino acids, then it would be predicted that MSG and l-amino acids elicit similar tastes in rats. The present study compared the taste profile of MSG with four amino acids (glycine, l-proline, l-serine and l-arginine) using conditioned taste aversion, detection threshold, and taste discrimination methods. These experiments were designed to either reduce or neutralize the taste of sodium associated with MSG and the other amino acids. Detection threshold studies showed that rats were most sensitive to l-arginine and least sensitive to l-proline. Glycine and l-serine thresholds were similar to those previously reported for MSG. Like MSG, a conditioned taste aversion to each of the four amino acids generalized to sucrose in the presence of amiloride, a sodium channel blocker. Rats showed moderate generalization of aversion between MSG and l-arginine, suggesting that these two amino acids taste only moderately alike. However, the taste aversion experiments indicated that glycine, l-serine, and l-proline elicit taste sensations similar to MSG when amiloride is present. Discrimination experiments further compared the tastes of these three amino acids with MSG. When the sodium taste associated with MSG was reduced or neutralized, glycine and l-proline elicited tastes very similar but not identical to the taste of MSG. Low (but not higher) concentrations of l-serine were also difficult for rats to discriminate from MSG. While there are taste qualities common to all of these amino acids, the perceptual differences found in this study, combined with previous reports, suggest either multiple taste receptors and/or multiple signaling pathways may be involved in umami and amino acid taste perception in rats.

Gastric bypass surgery restores altered neuronal coding for sweet taste in obese OLETF rats.

Otsuka Long-Evans Tokushima Fatty (OLETF) rats have a null mutation to the CCK-1 receptor and gradually develop obesity and type-2 diabetes. To date, the Roux-en-Y gastric bypass (GBP) surgery is the most successful intervention for weight loss. Based on observations in GBP patients suggesting altered food choices, and our previous findings showing that OLETF-GBP rats exhibit a reduced two bottle preference and a decreased lick-response to high concentrations of sucrose compared to sham-operated OLETF rats, in the present study we investigated the electrophysiological effects of GBP surgery on sucrose concentration coding in this strain. After GBP, obese OLETF rats lost and maintained body weight similar to that seen in human (−25 to 30%) and demonstrated improved glucose tolerance compared to pair-fed sham-operated OLETF rats. Extracellular single neuron recordings in the pontine parabrachial nucleus revealed that taste neurons of sham-operated OLETF rats with ad libitum access to food have an increased response function to higher concentrations of orally applied sucrose. This effect was reversed by GBP surgery. The relative distribution and response characteristics of neurons that best responded to sweet versus salty taste in OLETF-GBP but not in LETO-GBP rats were also altered by GBP. These findings demonstrate altered taste coding in this obese model and the capacity of GBP surgery to alleviate these impairments. A similar mechanism may be responsible for changes in eating habits and food choice reported in GBP human patients. Supported by NIH Grants DK065709, GM55639, PA-TS Fund, and PSU Diabetes Center Seed-Grant.

Expression of Aquaporin Water Channels in Rat Taste Buds

In order to gain insight into the molecular mechanisms that allow taste cells to respond to changes in their osmotic environment, we have used primarily immunocytochemical and molecular approaches to look for evidence of the presence of aquaporin-like water channels in taste cells. Labeling of isolated taste buds from the fungiform, foliate, and vallate papillae in rat tongue with antibodies against several of the aquaporins (AQPs) revealed the presence of AQP1, AQP2, and AQP5 in taste cells from these areas. AQP3 antibodies failed to label isolated taste buds from any of the papillae. There was an apparent difference in the regional localization of AQP labeling within the taste bud. Antibodies against AQP1 and AQP2 labeled predominantly the basolateral membrane, whereas the AQP5 label was clearly evident on both the apical and basolateral membranes of cells within the taste bud. Double labeling revealed that AQP1 and AQP2 labeled many, but not all, of the same taste cells. Similar double-labeling experiments with anti-AQP2 and anti-AQP5 clearly showed that AQP5 was expressed on or near the apical membranes whereas AQP2 was absent from this area. The presence of these 3 types of AQPs in taste buds but not in non-taste bud-containing epithelia was confirmed using reverse transcription-polymerase chain reaction. Experiments using patch clamp recording showed that the AQP inhibitor, tetraethylammonium, significantly reduced hypoosmotic-induced currents in rat taste cells. We hypothesize that the AQPs may play roles both in the water movement underlying compensatory mechanisms for changes in extracellular osmolarity and, in the case of AQP5 in particular, in the gustatory response to water.

Response properties of the pharyngeal branch of the glossopharyngeal nerve for umami taste in mice and rats

Many studies have reported the mechanism underlying umami taste. However, there are no investigations of responses to umami stimuli taste originating from chemoreceptors in the pharyngeal region. The pharyngeal branch of the glossopharyngeal nerve (GPN-ph) innervating the pharynx has unique responses to taste stimulation that differs from responses of the chorda tympani nerve and lingual branch of the glossopharyngeal nerve. Water evokes robust response, but NaCl solutions at physiological concentrations do not elicit responses. The present study was designed to examine umami taste (chemosensory) responses in the GPN-ph. Response characteristics to umami taste were compared between mice and rats. In mice, stimulation with compounds eliciting umami taste (0.1 M monosodium l-glutamate (MSG), 0.01 M inosine monophosphate (IMP) and the mixture of 0.1 M MSG + 0.01 M IMP) evoked higher responses than application of distilled water (DW). However, synergistic response of a mixture of 0.1 M MSG + 0.01 M IMP was not observed. In rats, there is no significant difference between the responses to umami taste (0.1 M MSG, 0.01 M IMP and the mixture of 0.1 M MSG + 0.01 M IMP) and DW. Monopotassium glutamate (MPG) was used in rats to examine the contribution of the sodium component of MSG on the response. Stimulation with 0.1 M MPG evoked a higher response when compared with responses to DW. The present results suggest that umami taste compounds are effective stimuli of the chemoreceptors in the pharynx of both mice and rats.

Expression of group II metabotropic glutamate receptors in rat gustatory papillae

Glutamate is one candidate for the neurotransmitters and/or neuromodulators involved in taste signaling in taste buds. Group II metabotropic glutamate receptors (mGluRs: mGluR2 and mGluR3) are known to function as presynaptic receptors that regulate the release of glutamate and/or other neurotransmitters in the central nervous system. Group II mGluRs are negatively linked to adenylyl cyclase through Galphai subunits and thereby reduce the turnover of cAMP. In rat taste tissues, a subset of adenylyl-cyclase-8-expressing taste cells coexpress the Galphai subunits gustducin and Galphai2. However, the expression patterns of group II mGluRs in rat taste tissues have not yet been elucidated. We have therefore examined the expression patterns of mGluR2, mGluR3, and gustducin in rat gustatory tissues. Reverse transcription/polymerase chain reaction assays have revealed that mGluR2 and mGluR3 mRNAs are expressed in the circumvallate papillae. In situ hybridization analyses have detected positive signals for mGluR2 and mGluR3 mRNAs only in the circumvallate taste buds. Among the fungiform, foliate, and circumvallate papillae, an antibody against mGluR2/3 labels a subset of taste bud cells and nerve fibers immediately beneath the taste lingual epithelium. Double-labeling experiments have demonstrated that mGluR2/3-positive cells coexpress gustducin. These results indicate that mGluR2 and mGluR3 are coupled to Galphai subunits and play roles in glutamate-mediated signaling in taste transductions.

Qualitative and quantitative differences between taste buds of the rat and mouse

BackgroundNumerous electrophysiological, ultrastructural, and immunocytochemical studies on rodent taste buds have been carried out on rat taste buds. In recent years, however, the mouse has become the species of choice for molecular and other studies on sensory transduction in taste buds. Do rat and mouse taste buds have the same cell types, sensory transduction markers and synaptic proteins? In the present study we have used antisera directed against PLCβ2, α-gustducin, serotonin (5-HT), PGP 9.5 and synaptobrevin-2 to determine the percentages of taste cells expressing these markers in taste buds in both rodent species. We also determined the numbers of taste cells in the taste buds as well as taste bud volume.ResultsThere are significant differences (p < 0.05) between mouse and rat taste buds in the percentages of taste cells displaying immunoreactivity for all five markers. Rat taste buds display significantly more immunoreactivity than mice for PLCβ2 (31.8% vs 19.6%), α-gustducin (18% vs 14.6%), and synaptobrevin-2 (31.2% vs 26.3%). Mice, however, have more cells that display immunoreactivity to 5-HT (15.9% vs 13.7%) and PGP 9.5 (14.3% vs 9.4%). Mouse taste buds contain an average of 85.8 taste cells vs 68.4 taste cells in rat taste buds. The average volume of a mouse taste bud (42,000 μm3) is smaller than a rat taste bud (64,200 μm3). The numerical density of taste cells in mouse circumvallate taste buds (2.1 cells/1000 μm3) is significantly higher than that in the rat (1.2 cells/1000 μm3).ConclusionThese results suggest that rats and mice differ significantly in the percentages of taste cells expressing signaling molecules. We speculate that these observed dissimilarities may reflect differences in their gustatory processing.

GPR expression in the rat taste bud relating to fatty acid sensing

We investigated the expression of G protein-coupled receptor GPR40 and GPR120 in the rat tongue. Using reverse transcription polymerase chain reaction, we detected a significant expression of GPR120 mRNA in the epithelium of the circumvallate papillae but not in the nonsensory epithelium, while the expression of GPR40 mRNA was undetectable in the sensory papillae. Western blotting analysis of colon and circumvallate papillae for GPR120 showed a protein band with a molecular weight that corresponds to that of GPR120, indicating that this antibody could recognize a native form of GPR120. Immunohistochemistry using anti-GPR120 antibody revealed GPR120 immunoreactivity in the enteroendocrine cells of the colon. Furthermore, some cells in each taste bud were stained positively with more intense labeling in the apical part of the cells. These results suggested that GPR120 is expressed in the taste cells of the circumvallate papillae to sense dietary fat, like the receptor expressed in the enteroendocrine cells.