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Results for “Taste Receptors, Type 2”

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PubMed1999

Physiological evidence for ionotropic and metabotropic glutamate receptors in rat taste cells.

Monosodium glutamate (MSG) elicits a unique taste in humans called umami. Recent molecular studies suggest that glutamate receptors similar to those in brain are present in taste cells, but their precise role in taste transduction remains to be elucidated. We used giga-seal whole cell recording to examine the effects of MSG and glutamate receptor agonists on membrane properties of taste cells from rat fungiform papillae. MSG (1 mM) induced three subsets of responses in cells voltage-clamped at -80 mV: a decrease in holding current (subset I), an increase in holding current (subset II), and a biphasic response consisting of an increase, followed by a decrease in holding current (subset III). Most subset II glutamate responses were mimicked by the ionotropic glutamate receptor (iGluR) agonist N-methyl-D-aspartate (NMDA). The current was potentiated by glycine and was suppressed by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5). The group III metabotropic glutamate receptor (mGluR) agonist L-2-amino-4-phosphonobutyric acid (L-AP4) usually mimicked the subset I glutamate response. This hyperpolarizing response was suppressed by the mGluR antagonist (RS)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG) and by 8-bromo-cAMP, suggesting a role for cAMP in the transduction pathway. In a small subset of taste cells, L-AP4 elicited an increase in holding current, resulting in taste cell depolarization under current clamp. Taken together, our results suggest that NMDA-like receptors and at least two types of group III mGluRs are present in taste receptor cells, and these may be coactivated by MSG. Further studies are required to determine which receptors are located on the apical membrane and how they contribute to the umami taste.

2-Amino-5-phosphonovalerate↗

PubMed2001

Acidic stimuli activates two distinct pathways in taste receptor cells from rat fungiform papillae.

A sour taste sensation may be produced when acidic stimuli interact with taste receptor cells (TRCs) on the dorsal surface of the tongue. We have searched for pathways in TRCs that may be activated by acidic stimuli using RT-PCR and changes in intracellular calcium (Ca(2+)(I)) induced by acidic stimuli in rat fungiform papillae. RT-PCR revealed the presence of proton-gated subunits ASIC-beta and VR1. Ca(2+) imaging measurements of the TRCs revealed two distinct responses to acidic stimuli: Ca(2+)(i) was increased in 9% (28/308; Type I) and was decreased in 39% (121/308; Type II). Neither of these responses was affected by the removal of extracellular Ca(2+), indicating that the changes arise from the release and sequestration of Ca(2+) from intracellular stores. These responses were also not inhibited by the vanilloid receptor antagonist, capsazepine, suggesting they do not arise from the activation of vanilloid receptors. The Type I, but not the Type II response was inhibited by amiloride. Dose-response measurements for Types I and II responses yielded pH(50%) of 4.8 and 4.9, respectively. Type II responses were inhibited by pertussis toxin, suggesting G-protein involvement. TRCs that exhibit Type II responses could also be activated by quinine (which increased Ca(2+)(I)) thus suggesting a mechanism by which the addition of acid may be suppressive to other chemical stimuli.

Acid Sensing Ion Channels↗

PubMed2004

[Stomatitis and ageusia induced by candesartan].

Cases of dysgeusia or ageusia have been reported in patients treated with angiotensin II receptor antagonist such as losartan (5 cases), valsartan (1 case), eprosartan (1 case). This is the first case-report of ageusia following candesartan. A 46-year-old-male patient, with a medical history of renal chronic reject allograft disease, started candesartan 4 mg once daily to treat high blood pressure. Six months later, a progressive ageusia occurred with a burning mouth syndrome. He also developed aphthous ulcers of the mouth, stomatitis and perleche, which led him to lose 8 kilos within 13 months. Thirteen months after the beginning of the treatment candesartan was stopped. The symptoms and lesions required 2 to 3 weeks to disappear. Subsequently, appetite was found again as well as the sense of taste. The temporal sequence of events suggests a causal relationship between ageusia and candesartan.

Ageusia↗

PubMed2003

MPEP, a selective metabotropic glutamate receptor 5 antagonist, attenuates conditioned taste aversion in rats.

Metabotropic glutamate receptors (mGluRs) have been implicated in several types of cognitive and associative learning. Although recent evidence indicates an influence of mGluRs in conditioned taste aversion (CTA), the subtype-specific involvement of mGluRs in this learning paradigm remained to be determined. The aim of this study was to examine the role of Group I mGluR subtypes in CTA using a selective mGluR5 antagonist (2-methyl-6-(phenylethynyl)-pyridine, MPEP) and a selective mGluR1 antagonist (1-aminoindan-1,5-dicarboxylic acid, AIDA). Male, water-deprived, Sprague-Dawley rats were injected i.p. with 6 or 12 mg/kg MPEP or saline. Twenty-five minutes later, all rats received 15-min access to a 0.1% saccharin solution (Sac) immediately followed by an injection of 0.15M LiCl at 1.33% body weight. The animals were tested with 15-min access to Sac on each of four test days. MPEP-treated animals consumed more Sac on the test trials than saline-treated rats. In another experiment, controlled access to Sac was used by infusing the solution on the conditioning trial. Consistent with the above results, MPEP attenuated the degree of CTA. Similar experiments using the mGluR1 antagonist AIDA, have found no effect on CTA learning. These results suggest that the two subtypes of Group I mGluRs are differentially involved in taste aversion learning.

Animals↗

PubMed1992

Apical K+ channels in Necturus taste cells. Modulation by intracellular factors and taste stimuli.

The apically restricted, voltage-dependent K+ conductance of Necturus taste receptor cells was studied using cell-attached, inside-out and outside-out configurations of the patch-clamp recording technique. Patches from the apical membrane typically contained many channels with unitary conductances ranging from 30 to 175 pS in symmetrical K+ solutions. Channel density was so high that unitary currents could be resolved only at negative voltages; at positive voltages patch recordings resembled whole-cell recordings. These multi-channel patches had a small but significant resting conductance that was strongly activated by depolarization. Patch current was highly K+ selective, with a PK/PNa ratio of 28. Patches containing single K+ channels were obtained by allowing the apical membrane to redistribute into the basolateral membrane with time. Two types of K+ channels were observed in isolation. Ca(2+)-dependent channels of large conductance (135-175 pS) were activated in cell-attached patches by strong depolarization, with a half-activation voltage of approximately -10 mV. An ATP-blocked K+ channel of 100 pS was activated in cell-attached patches by weak depolarization, with a half-activation voltage of approximately -47 mV. All apical K+ channels were blocked by the sour taste stimulus citric acid directly applied to outside-out and perfused cell-attached patches. The bitter stimulus quinine also blocked all channels when applied directly by altering channel gating to reduce the open probability. When quinine was applied extracellularly only to the membrane outside the patch pipette and also to inside-out patches, it produced a flickery block. Thus, sour and bitter taste stimuli appear to block the same apical K+ channels via different mechanisms to produce depolarizing receptor potentials.

Adenosine Triphosphate↗

PubMed2002

Urocortin in the lateral septal area modulates feeding induced by orexin A in the lateral hypothalamus.

The intermediate portion of the lateral septum (LSi) contains high levels of urocortin (UCN) peptide and type 2 corticotropin-releasing hormone (CRH) receptor (CRHR2) and has anatomic and functional connections with the lateral hypothalamus (LH). We tested the effect of UCN in the LSi on feeding. Injection of 10 or 30 pmol UCN into LSi significantly decreased feeding in food-deprived rats for 24 h without producing conditioned taste aversion (CTA). Pretreatment with a CRH receptor antagonist, alpha-helical CRH (alpha-hCRH), blocked the inhibitory effect of UCN on deprivation-induced feeding at 1 and 2 h postinjection. Furthermore, UCN in the LSi significantly decreased feeding induced by LH-injected orexin A at 2 and 4 h postinjection, and addition of alpha-hCRH blocked the inhibitory effect of UCN on orexin A-induced feeding. In conclusion, UCN significantly inhibits feeding induced by deprivation and LH-injected orexin A without producing a CTA, an effect that is mediated by CRHR2. These data define the LSi as an important site for UCN-induced anorexia and indicate that LSi UCN may influence orexin A feeding signals in the LH.

Animals↗

PubMed2005

Comparative study of taste disturbance by losartan and perindopril in healthy volunteers.

The aim of this study was to compare the degree of taste disturbance by losartan, an angiotensin II receptor blocker, with that of perindopril, an angiotensin-converting enzyme inhibitor. Perindopril erbumine (2 mg), losartan potassium (25 mg), or vehicle was given to Japanese volunteers (n = 7) for 14 days in a randomized, placebo-controlled, 3-way crossover design with a 14-day washout period. Gustometry by filter-paper test and electrogustometry were performed before and at the end of each trial. Plasma renin activity (PRA) and serum and salivary zinc concentrations were measured. One subject dropped out because of a perindopril-induced dry cough, but no one claimed a taste disturbance. Detection thresholds of 4 basic tastes (sweet, salty, sour, and bitter) by the paper-disc test and electrogustometry were significantly worsened, and plasma renin activity was elevated by the drugs, whereas the deteriorating effects of 2 drugs did not significantly differ. These drugs did not affect zinc concentrations in plasma and saliva. It was concluded that losartan and perindopril similarly alter taste sensitivity during repeated dosing of the drugs.

Adult↗

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↗

PubMed2005

Neural representation of bitter taste in the nucleus of the solitary tract.

Based on the molecular findings that many bitter taste receptors (T2Rs) are expressed within the same receptor cells, it has been proposed that bitter taste is encoded by the activation of discrete neural elements. Here we examined how a variety of bitter stimuli are represented by neural activity in central gustatory neurons. Taste responses (spikes/s) evoked by bathing the tongue and palate with intensity-matched concentrations (in M) of 2 sugars (0.32 sucrose and 0.5 D-fructose), ethanol (40%), 4 salts (0.01 NaCl, 0.008 NaNO(3), 0.01 MgCl(2), and 0.05 KCl), 2 acids (0.003 HCl and 0.005 citric acid), and 10 bitter ligands (0.007 quinine-HCl, 0.015 denatonium benzoate, 0.003 l-cysteine, 0.001 nicotine, 0.005 strychnine-HCl, 0.04 tetraethylammonium chloride, 0.03 atropine-SO(4), 0.005 brucine-SO(4), 0.03 papaverine-HCl, and 0.009 sparteine) were recorded from 51 neurons in the nucleus of the solitary tract of anesthetized rats. Cluster analysis was used to categorize neurons into types based on responses to sucrose, NaCl, HCl, and quinine-HCl. Three groupings emerged: type S (responded optimally to sweets), type N (sodium-optimal), and type H/Q (responded robustly to bitters, acids, and salts). Multivariate analyses revealed that across-neuron patterns of response among bitter stimuli were strongly correlated. However, neural type H/Q, which was most responsive to bitter tastants, was not differentially sensitive to bitter stimuli and Na(+) salts, which rats perceive as distinct. Thus central neurons most responsive to bitter substances receive significant input from receptors that mediate other tastes, indicating that bitter stimuli are not represented by activity in specifically tuned neurons.

Action Potentials↗

PubMedDate not supplied

Hyperphagic effect of B-HT 920 in a modified X-maze test.

The influence on rat-feeding behavior of B-HT 920 (a selective agonist of D2DA receptors at low doses, but also a potent stimulant of alpha 2-adrenoceptors at high doses) was examined using a new experimental model. The apparatus adopted was an X-maze with alternate open and covered arms, each baited with two food-pellets. Individual rats were placed in the apparatus and observed for 5 min. Two essential aspects of rat behavior in the presence of food were considered: tasting and feeding. A number of parameters were recorded: latency to tasting and feeding; interval between tasting and feeding; total feeding time. We also took into account the type of arm in which the rats indulged in their first bout of tasting and feeding. In the first series of experiments, B-HT 920 was injected intraperitoneally (0.1, 1, 2 and 3 mg/kg) into fed and fasted rats; in the second series, the drug was injected intracerebroventricularly (10, 20 and 80 micrograms/rat) into fasted rats. In both experimental conditions, the drug significantly modified the animals' feeding behavior and affected their natural preference for the closed arms as places of choice in which to feed. Comparison of the results with those obtained using norepinephrine (20 micrograms/rat, intracerebroventricularly), a well-known hyperphagic agent, shows that B-HT 920 strongly stimulates feeding. Also, the results of the intracerebroventricular experiments confirm that the effect on feeding appears at doses that are active both on alpha 2-adrenoceptors and on D2DA receptors, as can be deduced from penile erection and stretching and yawning elicited in rats by the same D2DA stimulant doses. The involvement of the latter receptors in feeding has been investigated by means of a new series of experiments with rats treated with the D2DA antagonist sulpiride, before B-HT 920 at 100 micrograms/kg. The possible mechanisms underlying B-HT 920-hyperphagic effects and the value of the X-maze feeding test as a simple procedure indicative of changes in rat feeding and emotionality are discussed in the light of these latest findings.

Adrenergic alpha-Agonists↗

PubMed1995

[Healing process of taste receptor disturbance].

Patients with taste receptor disturbance were treated with zinc dosage, and their healing process was traced through the filter-paper-disc method and electrogustometry. The number of cases studied was 119,45 with idiopathic taste disturbance, 38 with drug-induced taste disturbance and 36 with zinc-deficient taste disturbance. 1) Three patterns of taste recovery were observed on the tongue surface. Out of a total of 119 cases, 54 cases (45.4%) were found to be improving on the anterior as well as posterior parts of the tongue simultaneously (simultaneous improvement type). Fifty-three cases (44.5%) showed recovery in the posterior part of the tongue (area of the glossopharyngeal nerve) earlier than in other parts of the tongue (posterior improvement type). Only 12 cases (10.1%) showed recovery in the anterior part of the tongue (area of the chorda tympani nerve) earlier than in other parts of the tongue (anterior improvement type), a significantly smaller number of cases compared with the other two types. In particular, very few cases of zinc deficient taste disturbance belonged to the anterior improvement type. Zinc dosage treatment proved to be more rapidly effective for the simultaneous improvement type. 2) With respect to differences in the recovery process of the four primary tastes, a tendency for the sweet and bitter taste qualities to recover earlier than the others was observed in the simultaneous improvement type. However, no phenomenon was observed that could support the existence of the so-called "tongue map", such as the bitter and sour taste recover first among the posterior improvement type or the sweet taste improving first among the anterior improvement type. 3) The results of this study revealed that the treatment of taste receptor disturbances starts with the posterior part of the tongue, which abounds in taste buds. 4) The study also demonstrated that electrogustometry is not suitable for tracing the process of taste receptor disturbance. 5) When tracing the effectiveness of treatment of taste receptor disturbance through the filter paper-disc method, it is sufficient to measure only the posterior part of the tongue (area of the glossopharyngeal nerve) until signs of healing appear.

Adolescent↗

PubMed1999

Sweet taste responses of mouse chorda tympani neurons: existence of gurmarin-sensitive and -insensitive receptor components.

Inhibitory effects of gurmarin (gur) on responses to sucrose and other sweeteners of single fibers of the chorda tympani nerve in C57BL mice were examined. Of 30 single fibers that strongly responded to 0. 5 M sucrose but were not or to lesser extent responsive to 0.1 M NaCl, 0.01 M HCl, and 0.02 M quinine HCl (sucrose-best fibers), 16 fibers showed large suppression of responses to sucrose and other sweeteners by lingual treatment with 4.8 microM (approximately 20 microg/ml) gur (suppressed to 4-52% of control: gur-sensitive fibers), whereas the remaining 14 fibers showed no such gur inhibition (77-106% of control: gur-insensitive fibers). In gur-sensitive fibers, responses to sucrose inhibited by gur recovered to approximately 70% of control responses after rinsing the tongue with 15 mM beta-cyclodextrin and were almost abolished by further treatment with 2% pronase. In gur-insensitive fibers, sucrose responses were not inhibited by gur, but were largely suppressed by pronase. These results suggest existence of two different receptor components for sweeteners with different susceptibilities to gur in mouse taste cells, one gur sensitive and the other gur insensitive. Taste cells possessing each component may be specifically innervated by a particular type of chorda tympani neurons.

Animals↗

PubMed1990

Corpuscular bodies in the palate of the rat. 1. Morphology and distribution.

The morphology and the frequency distribution of corpuscular bodies in the palate was studied in rats using light and electron microscopy. The study extended from the day of birth through 180 days after birth. The corpuscles appeared as round (diameter 35-50 microns) to ovoid (width 40-60 microns, height 60-90 microns) bodies intercalated within the epithelium of the incisal papilla and the soft palate. A subepithelial nerve plexus surrounded the base of a corpuscle. For types of cells were identified within the corpuscle: basal, type I (dark), type II (pale) and type III cells. Some cells bore microvilli which protruded through a pore into the oral cavity. Numerous nerve endings terminated in close relation to the latter three types of cells. Two distinct types of membrane specializations were found representing axosomatic and axo-axonal contacts. On morphological grounds we interpret the structures described as receptors of taste. At birth, a mean total of 21 corpuscles was observed in the entire palate of which 31% was located on the incisal papilla and 68% was found in the soft palate. During the first 2 weeks (16 days) of postnatal life, the number of corpuscles increased. Thereafter, a significant decrease in corpuscle number occurred with increasing age. We speculate that the corpuscles are associated with the learning process of food selection.

Aging↗

PubMed2004

A specific receptor site for glycerol, a new sweet tastant for Drosophila: structure-taste relationship of glycerol in the labellar sugar receptor cell.

Glycerol, a linear triol, is a sweet tastant for mammals but it has not previously been recognized to stimulate the sense of taste in insects. Here we show by electrophysiological experimentation that it effectively stimulates the labellar sugar receptor cell of Drosophila. We also show that in accord with the electrophysiological observations, the behavioral feeding response to glycerol is dose dependent. 3-Amino-1,2-propanediol inhibited the response of the sugar receptor cell to glycerol, specifically and competitively, while it had almost no effect on responses to sucrose, D-glucose, D-fructose and trehalose. In the null Drosophila mutant for the trehalose receptor (DeltaEP19), the response to glycerol showed no change, in sharp contrast with a characteristic drastic decrease in the response to trehalose. The glycerol concentration-response curves for I-type and L-type labellar hairs were statistically indistinguishable, while those for sucrose, D-glucose, D-fructose and trehalose were clearly different. These all indicate the presence of a specific receptor site for glycerol. The glycerol site was characterized by comparing the effectiveness of various derivatives of glycerol. Based on this structure-taste relationship of glycerol, a model is proposed for the glycerol site including three subsites and two steric barriers, which cannot accommodate carbon-ring containing sugars such as D-glucose.

Animals↗

PubMed1993

The ionic basis of the receptor potential of frog taste cells induced by water stimuli.

The ionic mechanism underlying the receptor potential induced by a deionized water stimulus was studied in frog taste cells with conventional microelectrodes. The taste cells located in the proximal portion of the tongue generated a depolarizing receptor potential which averaged 10mV in response to stimulation with deionized water. The cell membrane of the water-sensitive taste cell could be divided into the taste-receptive (apical) and basolateral membranes and the cells were classified into two types: Cl(-)-dependent and Cl(-)-independent. In Cl(-)-dependent cells whose input resistance was decreased or unchanged by deionized water, the magnitude of the water-induced depolarization decreased with an increase in concentration of superficial Cl- in contact with the receptive membrane and with addition of blockers of anion channels (0.1 mmol l-1 SITS and 0.1 mmol l-1 DIDS) to deionized water. The reversal potential for the depolarization in this type shifted according to the concentration of superficial Cl-. These properties of the responses were consistent with those of the glossopharyngeal nerve which innervates the taste disc. In Cl(-)-independent cells whose input resistance was increased by deionized water, the reversal potential was approximately equal to the equilibrium potential for K+ at the basolateral membrane. The water-induced response of the glossopharyngeal nerve was decreased to about 60% of the control value by addition of interstitial 2 mmol l-1 Ba2+. It is concluded that the water-induced receptor potential is produced by Cl- secretion through the taste-receptive membrane in about 70% of water-sensitive frog taste cells, while it is generated by an inhibition of the resting K+ conductance of the basolateral membrane in the remaining 30% of the cells.

Action Potentials↗

PubMed1996

Characteristics of action potentials and their underlying outward currents in rat taste receptor cells.

1. Taste receptor cells produce action potentials as a result of transduction mechanisms that occur when these cells are stimulated with tastants. These action potentials are thought to be key signaling events in relaying information to the central nervous system. We explored the ionic basis of action potentials from dissociated posterior rat taste cells using the patch-clamp recording technique in both voltage-clamp and current-clamp modes. 2. Action potentials were evoked by intracellular injection of depolarizing current pulses from a holding potential of -80 mV. The threshold potential for firing of action potentials was approximately -35 mV; the input resistance of these cells averaged 6.9 G omega. With long depolarizing pulses, two or three action potentials could be elicited with successive attenuation of the spike height. Afterhyperpolarizations were observed often. 3. Both sodium and calcium currents contribute to depolarizing phases of the action potential. Action potentials were blocked completely in the presence of the sodium channel blocker tetrodotoxin. Calcium contributions could be visualized as prolonged calcium plateaus when repolarizing potassium currents were blocked and barium was used as a charge carrier. 4. Outward currents were composed of sustained delayed rectifier current, transient potassium current, and calcium-activated potassium current. Transient and sustained potassium currents activated close to -30 mV and increased monotonically with further depolarization. Up to half the outward current inactivated with decay constants on the order of seconds. Sustained and transient currents displayed steep voltage dependence in conductance and inactivation curves. Half inactivation occurred at -20 +/- 3.1 mV (mean +/- SE) with a decrease of 11.2 +/- 0.5 mV per e-fold. Half maximal conductance occurred at 3.6 +/- 1.8 mV and increased 12.2 +/- 0.6 mV per e-fold. Calcium-activated potassium current was evidenced by application of apamin and the use of calcium-free bathing solution. It was most obvious at more depolarized holding potentials that inactivated much of the transient and sustained outward currents. 5. Potassium currents contribute to both the repolarization and afterhyperpolarization phases of the action potential. These currents were blocked by bath application of tetraethylammonium, which also substantially broadened the action potential. Application of 4-aminopyridine was able to selectively block transient potassium currents without affecting sustained currents. This also broadened the action potential as well as eliminated the afterhyperpolarization. 6. A second type of action potential was observed that differed in duration. These slow action potentials had t1/2 durations of 9.6 ms compared with 1.4 ms for fast action potentials. Input resistances of the two groups were indistinguishable. Approximately one-fourth of the cells eliciting action potentials were of the slow type. 7. Cells eliciting fast action potentials had large outward currents capable of producing a quick repolarization, whereas cells with slow action potentials had small outward currents by comparison. The average values of fast cells were 2,563 pA and 1.4 ms compared with 373 pA and 9.6 ms for slow cells. Current and duration values were related exponentially. No significant difference was noted for inward currents. 8. These results suggest that many taste receptor cells conduct action potentials, which may be classified broadly into two groups on the basis of action potential duration and potassium current magnitude. These groups may be related to cell turnover. The physiological role of action potentials remains to be elucidated but may be important for communication within the taste bud as well as to the afferent nerve.

Action Potentials↗

PubMed1998

Taste preference in nonhuman primates to compounds sweet in man.

Primates have stimulated more interest than any other group as humans are ranked in this same mammalian order. Gustatory responses of human and nonhuman primates have already been compared for compounds such as monosaccharides, oligosaccharides, polyols, amino acids, dipeptides, proteins, dihydrochalcones, sulfamates, saccharin, acesulfame, diterpenes or urea derivatives, all known to be sweet in man. But no rational comparison in primates has been attempted. Using a structure-activity relationship study in primates, it is now possible to classify the primate sweetness receptors into four types according to the behavioral responses observed from various selected compounds sweet in humans. The four types are represented by (1) the Callitrichidae and (2) the Cebidae, both from the infraorder Platyrrhini (New World monkeys), (3) the Lemuridae and Lorisidae, from the suborder Prosimii (prosimians), and (4) the Cercopithecidae (Old World monkeys), Hylobatidae (lesser apes), Pongidae (great apes), and Hominidae (humans) from the infraorder Catarrhini (Old World simians). By a comparative study of the putative receptor recognition sites postulated for each type of receptor, it is inferred that the Callitrichidae (marmosets and tamarins) have retained the most primitive sweetness receptor among primates. As we believe that the evolution of the sweetness receptor is a key factor involved in the raising of nonhuman primates from a 'primitive grade' towards a more 'advanced' or 'simian grade,' the possible phylogenetic implications of these findings will be discussed.

Animals↗

PubMed2001

Acid detection by taste receptor cells.

Sourness is a primary taste quality that evokes an innate rejection response in humans and many other animals. Acidic stimuli are the unique sources of sour taste so a rejection response may serve to discourage ingestion of foods spoiled by acid producing microorganisms. The investigation of mechanisms by which acids excite taste receptor cells (TRCs) is complicated by wide species variability and within a species, apparently different mechanisms for strong and weak acids. The problem is further complicated by the fact that the receptor cells are polarized epithelial cells with different apical and basolateral membrane properties. The cellular mechanisms proposed for acid sensing in taste cells include, the direct blockage of apical K(+) channels by protons, an H(+)-gated Ca(2+) channel, proton conduction through apical amiloride-blockable Na(+) channels, a Cl(-) conductance blocked by NPPB, the activation of the proton-gated channel, BNC-1, a member of the Na(+) channel/degenerin super family, and by stimulus-evoked changes in intracellular pH. Acid-induced intracellular pH changes appear to be similar to those reported in other mammalian acid-sensing cells, such as type-I cells of the carotid body, and neurons found in the ventrolateral medulla, nucleus of the solitary tract, the medullary raphe, and the locus coceuleus. Like type-I carotid body cells and brainstem neurons, isolated TRCs demonstrate a linear relationship between intracellular pH (pH(i)) and extracellular pH (pH(o)) with slope, DeltapH(i)/DeltapH(o) near unity. Acid-sensing cells also appear to regulate pH(i) when intracellular pH changes occur under iso-extracellular pH conditions, but fail to regulate their pH when pH(i) changes are induced by decreasing extracellular pH. We shall discuss the current status of proposed acid-sensing taste mechanisms, emphasizing pH-tracking in receptor cells.

Acids↗