Receptive fields of sensory neurons in the brain are usually restricted to a portion of the entire stimulus domain. At all levels of the gustatory neuraxis, however, there are many cells that are broadly tuned, i.e., they respond well to each of the basic taste qualities (sweet, sour, salty and bitter). Although it might seem that this broad tuning precludes a major role for these cells in representing taste space, here we show the opposite – namely, that the tastant-specific temporal aspects (firing rate envelope and spike timing) of their responses enable each cell to represent the entire stimulus domain. Specifically, we recorded the response patterns of cells in the nucleus of the solitary tract (NTS) to representatives of four basic taste qualities and their binary mixtures. We analyzed the temporal aspects of these responses, and used their similarities and differences to construct the taste space represented by each neuron. We found that for the more broadly tuned neurons in the NTS, the taste space is a systematic representation of the entire taste domain. That is, the taste space of these broadly tuned neurons is three-dimensional, with basic taste qualities widely separated and binary mixtures placed close to their components. Further, the way that taste quality is represented by the firing rate envelope is consistent across the population of cells. Thus, the temporal characteristics of responses in the population of NTS neurons, especially those that are more broadly tuned, produce a comprehensive and logical representation of the taste world.
taste; nucleus of the solitary tract; temporal coding; gustation; electrophysiology; rat
It is becoming increasingly clear that the brain processes sensory stimuli differently according to whether they are passively or actively acquired, and these differences can be seen early in the sensory pathway. In the nucleus of the solitary tract (NTS), the first relay in the central gustatory neuraxis, a rich variety of sensory inputs generated by active licking converge. Here we show that taste responses in the NTS reflect these interactions. Experiments consisted of recordings of taste-related activity in the NTS of awake rats as they freely licked exemplars of the five basic taste qualities (sweet, sour, salty, bitter, umami). Nearly all taste-responsive cells were broadly tuned across taste qualities. A subset responded to taste with long latencies (>1.0 s), suggesting the activation of extra-oral chemoreceptors. Analyses of the temporal characteristics of taste responses showed that spike timing conveyed significantly more information than spike count alone in almost half of NTS cells, as in anesthetized rats, but with less information per cell. In addition to taste-responsive cells, the NTS contains cells that synchronize with licks. Since the lick pattern per se can convey information, these cells may collaborate with taste-responsive cells to identify taste quality. Other cells become silent during licking. These latter “anti-lick” cells show a surge in firing rate predicting the beginning and signaling the end of a lick bout. Collectively, the data reveal a complex array of cell types in the NTS, only a portion of which include taste-responsive cells, which work together to acquire sensory information.
It has been demonstrated that temporal features of spike trains can increase the amount of information available for gustatory processing. However, the nature of these temporal characteristics and their relationship to different taste qualities and neuron types are not well-defined. The present study analyzed the time course of taste responses from parabrachial (PBN) neurons elicited by multiple applications of “sweet” (sucrose), “salty” (NaCl), “sour” (citric acid), and “bitter” (quinine and cycloheximide) stimuli in an acute preparation. Time course varied significantly by taste stimulus and best-stimulus classification. Across neurons, the ensemble code for the three electrolytes was similar initially but quinine diverged from NaCl and acid during the second 500ms of stimulation and all four qualities became distinct just after 1s. This temporal evolution was reflected in significantly broader tuning during the initial response. Metric space analyses of quality discrimination by individual neurons showed that increases in information (H) afforded by temporal factors was usually explained by differences in rate envelope, which had a greater impact during the initial 2s (22.5% increase in H) compared to the later response (9.5%). Moreover, timing had a differential impact according to cell type, with between-quality discrimination in neurons activated maximally by NaCl or citric acid most affected. Timing was also found to dramatically improve within-quality discrimination (80% increase in H) in neurons that responded optimally to bitter stimuli (B-best). Spikes from B-best neurons were also more likely to occur in bursts. These findings suggest that among PBN taste neurons, time-dependent increases in mutual information can arise from stimulus- and neuron-specific differences in response envelope during the initial dynamic period. A stable rate code predominates in later epochs.
Psychophysical studies of interactions between retronasal olfaction and taste have focused most often on the enhancement of tastes by odors, which has been attributed primarily to a response bias (i.e., halo dumping). Based upon preliminary evidence that retronasal odors could also be enhanced by taste, the present study measured both forms of enhancement using appropriate response categories. In the first experiment, subjects rated taste (“sweet,” “sour,” “salty,” and “bitter”) and odor (“other”) intensity for aqueous samples of 3 tastants (sucrose, NaCl, and citric acid) and 3 odorants (vanillin, citral, and furaneol), both alone and in taste–odor mixtures. The results showed that sucrose, but not the other taste stimuli, significantly increased the perceived intensity of all 3 odors. Enhancement of tastes by odors was inconsistent and generally weaker than enhancement of odors by sucrose. A second experiment used a flavored beverage and a custard dessert to test whether the findings from the first experiment would hold for the perception of actual foods. Adding sucrose significantly enhanced the intensity of “cherry” and “vanilla” flavors, whereas adding vanillin did not significantly enhance the intensity of sweetness. It is proposed that enhancement of retronasal odors by a sweet stimulus results from an adaptive sensory mechanism that serves to increase the salience of the flavor of nutritive foods.
enhancement; flavor; psychophysics; retronasal odor; suppression; taste
The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. Here, we explored the logic of taste coding in the brain by examining how sweet, bitter, umami and saltiness are represented in the primary taste cortex. Using in vivo two-photon calcium-imaging we demonstrated striking topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.
Taste stimuli that evoke different perceptual qualities (e.g., sweet, umami, bitter, sour, salty) are detected by dedicated subpopulations of taste bud cells that employ distinct combinations of sensory receptors and transduction molecules. Here, we report that taste stimuli also elicit unique patterns of neuropeptide secretion from taste buds that are correlated with those perceptual qualities. We measured tastant-dependent secretion of glucagon-like peptide-1 (GLP-1), glucagon and neuropeptide Y (NPY) from circumvallate papillae of Tas1r3+/+, +/− and −/− mice. Isolated tongue epithelia were mounted in modified Ussing chambers, permitting apical stimulation of taste buds; secreted peptides were collected from the basal side and measured by specific ELISAs. Appetitive stimuli (sweet: glucose, sucralose; umami: monosodium glutamate; polysaccharide: Polycose) elicited GLP-1 and NPY secretion and inhibited basal glucagon secretion. Sweet and umami stimuli were ineffective in Tas1r3−/− mice, indicating an obligatory role for the T1R3 subunit common to the sweet and umami taste receptors. Polycose responses were unaffected by T1R3 deletion, consistent with the presence of a distinct polysaccharide taste receptor. The effects of sweet stimuli on peptide secretion also required the closing of ATP-sensitive K+ (KATP) channels, as the KATP channel activator diazoxide inhibited the effects of glucose and sucralose on both GLP-1 and glucagon release. Both sour citric acid and salty NaCl increased NPY secretion but had no effects on GLP-1 or glucagon. Bitter denatonium showed no effects on these peptides. Together, these results suggest that taste stimuli of different perceptual qualities elicit unique patterns of neuropeptide secretion from taste buds.
Although males and females differ in eating behavior and prevalence rates for eating disorders and obesity, little is known about gender differences in cortical activation to pleasant and unpleasant pure tastes during the physiological states of hunger and satiety. Twenty-one healthy young adults (12 females and 9 males) underwent two functional magnetic resonance imaging scans. Using four pure tastants of differing qualities (i.e., salty, sour, bitter, sweet), the present study examined gender differences in fMRI activation during two motivational states (hunger and satiety). There was greater change in fMRI activation from hunger to satiety in males than females in response to all tastes within the middle frontal gyrus (BA 10), insula, and cerebellum. Males also had greater change in activation from hunger to satiety, relative to females, in limbic regions including dorsal striatum, amygdala, parahippocampal gyrus, and posterior and anterior cingulate; however, activation was stimulus dependent, despite equivalent ratings in perceived pleasantness and intensity. Interestingly, males and females showed significant change from hunger to satiety in response to citric acid, suggesting that in addition to gender and physiological condition, stimulus quality is an important factor in taste fMRI activation. These gender differences may have implications for the pathophysiology of eating disorders and obesity.
Gender; Taste; Hunger; Satiety; Reward; fMRI
A longstanding question in taste research concerns taste coding and, in particular, how broadly are individual taste bud cells tuned to taste qualities (sweet, bitter, umami, salty, and sour). Taste bud cells express G-protein-coupled receptors for sweet, bitter, or umami tastes but not in combination. However, responses to multiple taste qualities have been recorded in individual taste cells. We and others have shown previously there are two classes of taste bud cells directly involved in gustatory signaling: “receptor” (type II) cells that detect and transduce sweet, bitter, and umami compounds, and “presynaptic” (type III) cells. We hypothesize that receptor cells transmit their signals to presynaptic cells. This communication between taste cells could represent a potential convergence of taste information in the taste bud, resulting in taste cells that would respond broadly to multiple taste stimuli. We tested this hypothesis using calcium imaging in a lingual slice preparation. Here, we show that receptor cells are indeed narrowly tuned: 82% responded to only one taste stimulus. In contrast, presynaptic cells are broadly tuned: 83% responded to two or more different taste qualities. Receptor cells responded to bitter, sweet, or umami stimuli but rarely to sour or salty stimuli. Presynaptic cells responded to all taste qualities, including sour and salty. These data further elaborate functional differences between receptor cells and presynaptic cells, provide strong evidence for communication within the taste bud, and resolve the paradox of broad taste cell tuning despite mutually exclusive receptor expression.
taste bud; cell type; taste processing; presynaptic cell; receptor cell; coding
The sense of taste is important for providing animals with valuable information about the qualities of food, such as nutritional or harmful nature. Mammals, including humans, can recognize at least five primary taste qualities: sweet, umami (savory), bitter, sour, and salty. Recent studies have identified molecules and mechanisms underlying the initial steps of tastant-triggered molecular events in taste bud cells, particularly the requirement of increased cytosolic free Ca2+ concentration ([Ca2+]c) for normal taste signal transduction and transmission. Little, however, is known about the mechanisms controlling the removal of elevated [Ca2+]c from the cytosol of taste receptor cells (TRCs) and how the disruption of these mechanisms affects taste perception. To investigate the molecular mechanism of Ca2+ clearance in TRCs, we sought the molecules involved in [Ca2+]c regulation using a single-taste-cell transcriptome approach. We found that Serca3, a member of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) family that sequesters cytosolic Ca2+ into endoplasmic reticulum, is exclusively expressed in sweet/umami/bitter TRCs, which rely on intracellular Ca2+ release for signaling. Serca3-knockout (KO) mice displayed significantly increased aversive behavioral responses and greater gustatory nerve responses to bitter taste substances but not to sweet or umami taste substances. Further studies showed that Serca2 was mainly expressed in the T1R3-expressing sweet and umami TRCs, suggesting that the loss of function of Serca3 was possibly compensated by Serca2 in these TRCs in the mutant mice. Our data demonstrate that the SERCA family members play an important role in the Ca2+ clearance in TRCs and that mutation of these proteins may alter bitter and perhaps sweet and umami taste perception.
Coding of the complex tastes of ionic stimuli in humans was studied by combining taste confusion matrix (TCM) methodology and treatment with chlorhexidine gluconate. The TCM evaluates discrimination of multiple stimuli simultaneously. Chlorhexidine, a bis-biguanide antiseptic, reversibly inhibits salty taste and tastes of a subset of bitter stimuli, including quinine hydrochloride. Identifications of salty (NaCl, “salt”), bitter (quinine·HCl, “quinine”), sweet (sucrose, “sugar”), and sour (citric acid, “acid”) prototypes, alone and as components of binary mixtures, were measured under 4 conditions. One was a water-rinse control and the others had the salt and quinine tastes progressively reduced by treatment with 1 mM chlorhexidine, 3 mM chlorhexidine, and ultimately to zero by elimination of NaCl and quinine·HCl. Treatment with chlorhexidine perturbed identification of salt more than quinine; both were thereafter more often confused with “water” and unidentified when mixed with sucrose or citric acid. All pairwise discriminations that depended on the tastes of NaCl and quinine·HCl deteriorated, and although H2O was mistakenly identified as quinine after chlorhexidine, this may have been a decisional bias. Other confusions reflected “unprompted mixture analysis” and an obscuring of salt taste by a less-inhibited stronger quinine or sugar or acid tastes in mixtures. Partial inhibition of the tastes of NaCl and quinine·HCl by chlorhexidine was considered in the context of multiple receptors for the 2 compounds. Discrimination among prototypic stimuli with varying strengths was consistent with a gustatory system that evaluates a small number of independent tastes.
binary mixtures; dynamic mixture analysis; mixture suppression; quinine inhibition; salt inhibition; taste confusion matrix
Psychophysical judgments often depend on stimulus context. For example, sugar solutions are judged sweeter when a tasteless fruity aroma has been added. Response context also matters; adding a fruity aroma to sugar increases the rated sweetness when only sweetness is considered but not when fruitiness is judged as well. The interaction between stimulus context and response context has been explored more extensively in taste–odor mixtures than in taste–taste mixtures. To address this issue, subjects in the current study rated the sourness of citric acid mixed with quinine (bitter), sodium chloride (salty), and cyclamate (sweet) (stimulus context). In one condition, subjects rated sourness alone. In another, subjects rated both sourness and the other salient quality (bitterness, saltiness, or sweetness) (response context). Sourness ratings were most sensitive to response context for sour–salty mixtures (i.e., ratings of sourness alone exceeded ratings of sourness made simultaneously with saltiness) and least sensitive to context for the sour–sweet mixtures (sourness ratings made under the 2 conditions were essentially identical). Response-context effects for the sour–bitter mixture were nominally intermediate. The magnitudes of these context effects were related to judgments of qualitative similarity between citric acid and the other stimuli, consistent with prior findings. These types of context effects are relevant to the study of taste–taste mixture interactions and should provide insight into the perceptual similarities among the taste qualities.
gustatory; psychophysics; similarity
In the tongue, distinct classes of taste receptor cells detect the five basic tastes, sweet, sour, bitter, sodium salt, and umami1,2. Among these qualities, bitter and sour stimuli are innately aversive, whereas sweet and umami are appetitive, and generally attractive to animals. In contrast, salty taste is unique in that increasing salt concentration fundamentally transforms an innately appetitive stimulus into a powerfully aversive one3–7. This appetitive-aversive balance helps maintain appropriate salt consumption3,4,6,8, and represents an important part of fluid and electrolyte homeostasis. We have previously shown that the appetitive responses to NaCl are mediated by taste receptor cells expressing the epithelial sodium channel, ENaC8, while the cellular substrate for salt aversion was unknown. Here we explore the cellular and molecular basis for the rejection of high concentrations of salts (>300 mM NaCl or KCl). We now show that high-salt recruits the two primary aversive taste pathways by activating the sour and bitter taste-sensing cells. We also demonstrate that genetic silencing of these pathways abolishes behavioral aversion to concentrated salt, without impairing salt attraction. Notably, mice devoid of salt-aversion pathways now exhibit unimpeded, continuous attraction even to exceedingly high concentrations of NaCl. We propose that the “co-opting” of sour and bitter neural pathways evolved as a means to ensure that high levels of salt reliably trigger robust behavioral rejection, thus preventing its potentially detrimental effects in health and well-being.
Mammals taste many compounds yet use a sensory palette consisting of only five basic taste modalities: sweet, bitter, sour, salty, and umami (the taste of monosodium glutamate)1,2. While this repertoire may appear modest, it provides animals with critical information about the nature and quality of food. Sour taste detection functions as an important sensory input to warn against the ingestion of acidic (e.g. spoiled or unripe) food sources1–3. We have used a combination of bioinformatics, genetic, and functional studies to identify PKD2L1, a polycystic kidney disease-like ion channel4, as a candidate mammalian sour taste sensor. In the tongue, PKD2L1 is expressed in a subset of taste receptor cells (TRCs) distinct from those responsible for sweet, bitter and umami taste. To examine the role of PKD2L1-expressing taste cells in vivo, we engineered mice with targeted genetic ablations of selected populations of TRCs. Animals lacking PKD2L1-cells are completely devoid of taste responses to sour stimuli. Notably, responses to all other tastants remained unaffected, proving that the segregation of taste qualities even extends to ionic stimuli. Our results now establish independent cellular substrates for four of the five basic taste modalities, and support a comprehensive labeled-line mode of taste coding at the periphery5–10. Interestingly, PKD2L1 is also expressed in specific neurons surrounding the central canal of the spinal cord. Here we demonstrate that these PKD2L1-expressing neurons send projections to the central canal, and selectively trigger action potentials in response to decreases in extracellular pH. We propose that these cells correspond to the long sought components of the cerebrospinal fluid chemosensory system11. Taken together, our results suggest a common basis for acid sensing in disparately different physiological settings.
Taste bud cells transmit information regarding the contents of food from taste receptors embedded in apical microvilli to gustatory nerve fibers innervating basolateral membranes. In particular, taste cells depolarize, activate voltage-gated sodium channels, and fire action potentials in response to tastants. Initial cell depolarization is attributable to sodium influx through TRPM5 in sweet, bitter, and umami cells and an undetermined cation influx through an ion channel in sour cells expressing PKD2L1, a candidate sour taste receptor. The molecular identity of the voltage-gated sodium channels that sense depolarizing signals and subsequently initiate action potentials coding taste information to gustatory nerve fibers is unknown.
We describe the molecular and histological expression profiles of cation channels involved in electrical signal transmission from apical to basolateral membrane domains. TRPM5 was positioned immediately beneath tight junctions to receive calcium signals originating from sweet, bitter, and umami receptor activation, while PKD2L1 was positioned at the taste pore. Using mouse taste bud and lingual epithelial cells collected by laser capture microdissection, SCN2A, SCN3A, and SCN9A voltage-gated sodium channel transcripts were expressed in taste tissue. SCN2A, SCN3A, and SCN9A were expressed beneath tight junctions in subsets of taste cells. SCN3A and SCN9A were expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells. HCN4, a gene previously implicated in sour taste, was expressed in PKD2L1 cells and localized to cell processes beneath the taste pore.
SCN2A, SCN3A and SCN9A voltage-gated sodium channels are positioned to sense initial depolarizing signals stemming from taste receptor activation and initiate taste cell action potentials. SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells.
The perception of sour taste in humans is incompletely understood at the receptor cell level. We report here on two patients with an acquired sour ageusia. Each patient was unresponsive to sour stimuli, but both showed normal responses to bitter, sweet, and salty stimuli.
Methods and Findings
Lingual fungiform papillae, containing taste cells, were obtained by biopsy from the two patients, and from three sour-normal individuals, and analyzed by RT-PCR. The following transcripts were undetectable in the patients, even after 50 cycles of amplification, but readily detectable in the sour-normal subjects: acid sensing ion channels (ASICs) 1a, 1β, 2a, 2b, and 3; and polycystic kidney disease (PKD) channels PKD1L3 and PKD2L1. Patients and sour-normals expressed the taste-related phospholipase C-β2, the δ-subunit of epithelial sodium channel (ENaC) and the bitter receptor T2R14, as well as β-actin. Genomic analysis of one patient, using buccal tissue, did not show absence of the genes for ASIC1a and PKD2L1. Immunohistochemistry of fungiform papillae from sour-normal subjects revealed labeling of taste bud cells by antibodies to ASICs 1a and 1β, PKD2L1, phospholipase C-β2, and δ-ENaC. An antibody to PKD1L3 labeled tissue outside taste bud cells.
These data suggest a role for ASICs and PKDs in human sour perception. This is the first report of sour ageusia in humans, and the very existence of such individuals (“natural knockouts”) suggests a cell lineage for sour that is independent of the other taste modalities.
Basic taste qualities like sour, salty, sweet, bitter and umami serve specific functions in identifying food components found in the diet of humans and animals, and are recognized by proteins in the oral cavity. Recognition of bitter taste and aversion to it are thought to protect the organism against the ingestion of poisonous food compounds, which are often bitter. Interestingly, bitter taste receptors are expressed not only in the mouth but also in extraoral tissues, such as the gastrointestinal tract, indicating that they may play a role in digestive and metabolic processes. BitterDB database, available at http://bitterdb.agri.huji.ac.il/bitterdb/, includes over 550 compounds that were reported to taste bitter to humans. The compounds can be searched by name, chemical structure, similarity to other bitter compounds, association with a particular human bitter taste receptor, and so on. The database also contains information on mutations in bitter taste receptors that were shown to influence receptor activation by bitter compounds. The aim of BitterDB is to facilitate studying the chemical features associated with bitterness. These studies may contribute to predicting bitterness of unknown compounds, predicting ligands for bitter receptors from different species and rational design of bitterness modulators.
Taste related information reaches the gustatory cortex (GC) through two routes: a thalamic and a limbic pathway. While evidence is accumulating on limbic-cortical interactions in taste, very little information is available on the function of the gustatory thalamus in shaping GC activity. Here we rely on behavioral electrophysiological techniques to study taste-evoked activity in GC before and after inactivation of the parvicellular portion of the ventroposteromedial nucleus of thalamus (VPMpc; i.e. the gustatory thalamus). Gustatory stimuli were presented to rats either alone or preceded by an anticipatory cue. The reliance on two different behavioral contexts allowed us to investigate how the VPMpc mediates GC responses to uncued tastants, cued tastants and anticipatory cues. Inactivation of the thalamus resulted in a dramatic reduction of taste processing in GC. However, responses to anticipatory cues were unaffected by this manipulation. The use of a cue-taste association paradigm also allowed for the identification of two subpopulations of taste specific neurons: those that responded to gustatory stimulation and to the cue (i.e. cue-and-taste) and those that responded to tastants only (i.e. taste-only). Analyses of these two populations revealed differences in response dynamics and connectivity with the VPMpc.
The results provide novel evidence for the role of VPMpc in shaping GC activity and demonstrate a previously unknown association between responsiveness to behavioral events, temporal dynamics and thalamic connectivity in GC.
The molecular machinery for chemosensory transduction in taste buds has received considerable attention within the last decade. Consequently, we now know a great deal about sweet, bitter, and umami taste mechanisms and are gaining ground rapidly on salty and sour transduction. Sweet, bitter, and umami tastes are transduced by G-protein-coupled receptors. Salty taste may be transduced by epithelial Na channels similar to those found in renal tissues. Sour transduction appears to be initiated by intracellular acidification acting on acid-sensitive membrane proteins. Once a taste signal is generated in a taste cell, the subsequent steps involve secretion of neurotransmitters, including ATP and serotonin. It is now recognized that the cells responding to sweet, bitter, and umami taste stimuli do not possess synapses and instead secrete the neurotransmitter ATP via a novel mechanism not involving conventional vesicular exocytosis. ATP is believed to excite primary sensory afferent fibers that convey gustatory signals to the brain. In contrast, taste cells that do have synapses release serotonin in response to gustatory stimulation. The postsynaptic targets of serotonin have not yet been identified. Finally, ATP secreted from receptor cells also acts on neighboring taste cells to stimulate their release of serotonin. This suggests that there is important information processing and signal coding taking place in the mammalian taste bud after gustatory stimulation.
Taste bud; Transduction; ATP; Serotonin; Neurotransmitters; Sweet; Bitter; Umami; Salty; Sour
Taste plays a crucial role in the life of honey bees as their survival depends on the collection and intake of nectar and pollen, and other natural products. Here we studied the tarsal taste of honey bees through a series of behavioral and electrophysiological analyses. We characterized responsiveness to various sweet, salty and bitter tastants delivered to gustatory sensilla of the fore tarsi. Behavioral experiments showed that stimulation of opposite fore tarsi with sucrose and bitter substances or water yielded different outcomes depending on the stimulation sequence. When sucrose was applied first, thereby eliciting proboscis extension, no bitter substance could induce proboscis retraction, thus suggesting that the primacy of sucrose stimulation induced a central excitatory state. When bitter substances or water were applied first, sucrose stimulation could still elicit proboscis extension but to a lower level, thus suggesting central inhibition based on contradictory gustatory input on opposite tarsi. Electrophysiological experiments showed that receptor cells in the gustatory sensilla of the tarsomeres are highly sensitive to saline solutions at low concentrations. No evidence for receptors responding specifically to sucrose or to bitter substances was found in these sensilla. Receptor cells in the gustatory sensilla of the claws are highly sensitive to sucrose. Although bees do not possess dedicated bitter-taste receptors in the tarsi, indirect bitter detection is possible because bitter tastes inhibit sucrose receptor cells of the claws when mixed with sucrose solution. By combining behavioral and electrophysiological approaches, these results provide the first integrative study on tarsal taste detection in the honey bee.
taste; gustation; gustatory receptors; insect; honey bee; tarsi; proboscis extension reflex; electrophysiology
Functional diversification of taste cells is crucial for proper discrimination of taste qualities. We found homeodomain protein Skn-1a/Pou2f3 is expressed in sweet, umami, and bitter taste cells. The Skn-1a–deficient mice lacked electrophysiological and behavioral responses to sweet, umami, and bitter tastes, due to complete absence of sweet, umami, and bitter cells with concomitant expansion of sour cells. Skn-1a is critical for generating and balancing the diverse composition of taste cells.
When a taste stimulus enters the mouth, intentional movement of the stimulus within the oropharyngeal cavity affects the rate at which taste receptors are exposed to the stimulus and may ultimately affect taste perception. Early studies have shown that stimulus flow rate, the experimental equivalent of the effects of these investigative movements, modulates the portion of the peripheral nerve response that occurs when behavioral assessments of tastants are made. The present experiment studied the neural coding mechanisms for flow rate in the nucleus of the solitary tract (NTS), the first central relay in the taste pathway. Responses to NaCl (0.1 M) presented at high (5 ml/s) and low (3 ml/s) flow rates, sucrose (0.5 M), quinine HCl (0.01 M), and HCl (0.01 M) were recorded extracellularly from single NTS units in multiple replications. Information conveyed by evoked responses was analyzed with a family of metrics that quantify the similarity of two spike trains in terms of spike count and spike timing. Information about flow rate was conveyed by spike timing and spike count in approximately equal proportions of units (each ∼1/3), whereas information about taste quality was conveyed by spike timing in about half of the units. Different subsets of units contributed information for discrimination of flow rate and taste quality.
Taste is a chemical sense responding to chemical stimuli. In our daily practice as ENT practitioners or Neurologists we do come across patients complaining of taste disturbances. Tests for taste have to be performed regularly in the clinical centres as well as in neurological labs as a part of complete work up for neurotology cases. Assessment of taste sensation can be easily done in a neurological clinic by chemogustometry as described by Claussen. The stimuli used are chemicals, representative substances for the four qualities of sweet, salty, sour and bitter, in graded solutions. These semi-quantitative results are plotted on a pentagon scheme devised by Claussen. The points of the best results for glucose, sodium chloride, citric acid, phenylthio-urea and quinine then are connected with a coloured line. That gives a linked graphic structure, which can be read by the physician at one glance. Different patterns are obtained for normal taste, taste-blindness for phenylthio-urea, ageusia, partial ageusias for glucose, or sodium chloride or citric acid or quinine or their combinations and parageusias. In this article we present different patterns of taste disturbances depicted on the pentagon chart highlighting the easy interpretation of chemogustometry.
Chemogustometry; Taste; Pentagon chart; Ageusia; Parageusia
There is emerging evidence that two parallel lines of gustatory information are generated in taste buds. One pathway leads to higher cortical centers and is involved in discriminating basic taste qualities (sweet, bitter, sour, salty, umami) and perceiving flavors. The other pathway may conduct information involved in physiological reflexes such as swallowing, salivation, and cephalic phase digestion. If this notion is true, the existence of two populations of taste bud cells that have different functional characteristics may lie at the origins of the two pathways. This speculative concept is explored in this review of taste signal processing in mammalian taste buds.
Taste transmitters; ATP; Serotonin; 5-HT; Noradrenalin; Pannexin 1; Cephalic phase digestion; Taste receptor cells; Taste bud synapses
To qualify as a “basic” taste quality or modality, defined as a group of chemicals that taste alike, three empirical benchmarks have commonly been used. The first is that a candidate group of tastants must have a dedicated transduction mechanism in the peripheral nervous system. The second is that the tastants evoke physiological responses in dedicated afferent taste nerves innervating the oropharyngeal cavity. Last, the taste stimuli evoke activity in central gustatory neurons, some of which may respond only to that group of tastants. Here we argue that water may also be an independent taste modality. This argument is based on the identification of a water dedicated transduction mechanism in the peripheral nervous system, water responsive fibers of the peripheral taste nerves and the observation of water responsive neurons in all gustatory regions within the central nervous system. We have described electrophysiological responses from single neurons in nucleus of the solitary tract (NTS) and parabrachial nucleus of the pons, respectively the first two central relay nuclei in the rodent brainstem, to water presented as a taste stimulus in anesthetized rats. Responses to water were in some cases as robust as responses to other taste qualities and sometimes occurred in the absence of responses to other tastants. Both excitatory and inhibitory responses were observed. Also, the temporal features of the water response resembled those of other taste responses. We argue that water may constitute an independent taste modality that is processed by dedicated neural channels at all levels of the gustatory neuraxis. Water-dedicated neurons in the brainstem may constitute key elements in the regulatory system for fluid in the body, i.e., thirst, and as part of the swallowing reflex circuitry.
taste; gustatory; water; nucleus of the solitary tract; parabrachial nucleus of the pons
Behavioral and electrophysiological studies suggest that rats can identify a taste stimulus with a single lick, in <200 ms. However, the conditions under which these conclusions were drawn varied widely across experiments. We designed a series of experiments to assess the effects of the number of licks of a tastant that are available, tastant concentration and prior learning experience on the speed with which a tastant can modify behavior. To accomplish this we tested exemplars of four basic taste qualities (quinine, 0.1 mM; NaCl, 100 mM; saccharin, 4 mM, or sucrose, 100 mM; citric acid, 10 mM) in rats that were conditioned to avoid quinine. Taste stimuli were available for one, two, or three licks on separate days. All tastants were presented in a randomized order interspersed with water rinse licks presented on a variable ratio schedule. A tastant-specific significant increase in the proportion of long pauses in licking following quinine presentation was defined as evidence of “behavioral identification.” Rats with aversion training given three licks of all taste stimuli paused significantly more often after quinine by the fourth interlick interval, ~580 ms. Control rats showed no evidence of quinine (0.1 mM) identification. When rats in all conditioning groups were tested with a high concentration of quinine (10 mM), a single lick was sufficient to produce significant pausing after quinine, but not until the fourth interlick interval, i.e., ~580 ms. Testing rats with only two tastants rather than four in a session had no effect on the speed of quinine identification. Present data confirm that a single lick is sufficient for rats to identify a taste stimulus, but that additional licks occur before evidence of identification is apparent. Furthermore, learning, tastant concentration and motivation to drink can all modify the speed of behavioral identification.
taste; identification; behavior; conditioned taste aversion; rat