Umami Stimuli Research Articles

Umami Altering Salivary Proteome: A Study across a Sensitivity Spectrum on Subjects.

This study delved into the relationship between umami taste sensitivity (UTS) and variations in the salivary proteome among 12 healthy nonsmokers utilizing 4D data-independent acquisition-based proteomics. By assessing UTS through monosodium l-glutamate (MSG) detection thresholds, we discovered notable differences: individuals with high UTS detected umami at significantly lower MSG concentrations (0.20 ± 0.12 mM) compared to their low UTS counterparts (2.51 ± 1.21 mM). Both groups showed an upregulation of the S100A1 protein under MSG stimulation, indicating a potent biochemical response to umami stimuli. The high UTS group exhibited enhanced metabolic pathways including those for amino acid, lipid, and organic acid biosynthesis, essential for maintaining taste receptor functionality and enhancing signal transduction. This group also demonstrated increased activity in cytochrome P450 enzymes and ribonucleoprotein complexes, suggesting a readiness to manage metabolic challenges and optimize umami perception. In contrast, the low UTS group showed adaptive mechanisms, possibly through modulation of receptor availability and function, with an upregulation of structural and ribosomal proteins that may support taste receptor production and turnover. These findings suggest that varying biological mechanisms underpin differences in umami perception, which could significantly influence dietary preferences and nutritional outcomes, highlighting the intricate interplay of genetic, physiological, and metabolic factors in taste sensitivity.

Altered peripheral taste function in a mouse model of inflammatory bowel disease

Increased sugar intake and taste dysfunction have been reported in patients with inflammatory bowel disease (IBD), a chronic disorder characterized by diarrhea, pain, weight loss and fatigue. It was previously unknown whether taste function changes in mouse models of IBD. Mice consumed dextran sodium sulfate (DSS) during three 7-day cycles to induce chronic colitis. DSS-treated mice displayed signs of disease, including significant weight loss, diarrhea, loss of colon architecture, and inflammation of the colon. After the last DSS cycle we assessed taste function by recording electrophysiological responses from the chorda tympani (CT) nerve, which transmits activity from lingual taste buds to the brain. DSS treatment significantly reduced neural taste responses to natural and artificial sweeteners. Responses to carbohydrate, salt, sour or bitter tastants were unaffected in mice with colitis, but umami responses were modestly elevated. DSS treatment modulated the expression of receptor subunits that transduce sweet and umami stimuli in oral taste buds as a substrate for functional changes. Dysregulated systemic cytokine responses or dysbiosis that occurs during chronic colitis may be upstream from changes in oral taste buds. We demonstrate for the first time that colitis alters taste input to the brain, which could exacerbate malnutrition in IBD patients.

EGR4 is critical for cell-fate determination and phenotypic maintenance of geniculate ganglion neurons underlying sweet and umami taste

The sense of taste starts with activation of receptor cells in taste buds by chemical stimuli which then communicate this signal via innervating oral sensory neurons to the CNS. The cell bodies of oral sensory neurons reside in the geniculate ganglion (GG) and nodose/petrosal/jugular ganglion. The geniculate ganglion contains two main neuronal populations: BRN3A+ somatosensory neurons that innervate the pinna and PHOX2B+ sensory neurons that innervate the oral cavity. While much is known about the different taste bud cell subtypes, considerably less is known about the molecular identities of PHOX2B+ sensory subpopulations. In the GG, as many as 12 different subpopulations have been predicted from electrophysiological studies, while transcriptional identities exist for only 3 to 6. Importantly, the cell fate pathways that diversify PHOX2B+ oral sensory neurons into these subpopulations are unknown. The transcription factor EGR4 was identified as being highly expressed in GG neurons. EGR4 deletion causes GG oral sensory neurons to lose their expression of PHOX2B and other oral sensory genes and up-regulate BRN3A. This is followed by a loss of chemosensory innervation of taste buds, a loss of type II taste cells responsive to bitter, sweet, and umami stimuli, and a concomitant increase in type I glial-like taste bud cells. These deficits culminate in a loss of nerve responses to sweet and umami taste qualities. Taken together, we identify a critical role of EGR4 in cell fate specification and maintenance of subpopulations of GG neurons, which in turn maintain the appropriate sweet and umami taste receptor cells.

Defining the role of TRPM4 in broadly responsive taste receptor cells.

Peripheral taste receptor cells use multiple signaling pathways to transduce taste stimuli into output signals that are sent to the brain. We have previously identified a subpopulation of Type III taste cells that are broadly responsive (BR) and respond to multiple taste stimuli including bitter, sweet, umami, and sour. These BR cells use a PLCβ3/IP3R1 signaling pathway to detect bitter, sweet, and umami stimuli and use a separate pathway to detect sour. Currently, the downstream targets of the PLCβ3 signaling pathway are unknown. Here we identify TRPM4, a monovalent selective TRP channel, as an important downstream component in this signaling pathway. Using live cell imaging on isolated taste receptor cells from mice, we show that inhibition of TRPM4 abolished the taste-evoked sodium responses and significantly reduced the taste-evoked calcium responses in BR cells. Since BR cells are a subpopulation of Type III taste cells, they have conventional chemical synapses that require the activation of voltage-gated calcium channels (VGCCs) to cause neurotransmitter release. We found that TRPM4-dependent membrane depolarization selectively activates L-type VGCCs in these cells. The calcium influx through L-type VGCCs also generates a calcium-induced calcium release (CICR) via ryanodine receptors that enhances TRPM4 activity. Together these signaling events amplify the initial taste response to generate an appropriate output signal.

Investigating the Influence of Different Umami Tastants on Brain Perception via Scalp Electroencephalogram.

Three types of tastants are known as perceptually associated with umami taste: monosodium glutamate (MSG), disodium succinate (WSA), and disodium inosine monophosphate (IMP). While these tastants were confirmed to be perceptually similar in a sensory study, they could be discriminated (p < 0.05) by electroencephalogram (EEG) analysis on a time scale of 5-6 s. In comparison of the EEG responses of the participants, the brain could partly distinguish (p < 0.05) between different sensory intensities of MSG, WSA, or IMP. The EEG data indicated that the brain is partially sensitive to perceiving different sensory intensities (L, low; M, medium; and H, high) of the same umami stimuli; i.e., for MSG in μV2/Hz, L, 2.473 ± 0.181; M, 3.274 ± 0.181; and H, 3.202 ± 0.181. However, brain responses of perceptually equi-umami intensities could partially be discriminated, suggesting that the brain could partially discriminate (p < 0.05) MSG, WSA, and IMP, despite similar sensory intensities. Moreover, umami tastants were also found to significantly enhance (p < 0.05) the α wave activity, with the most responsive being at 10 Hz, particularly in the frontal and parietal and occipital regions of the brain (p < 0.001). This study shows the potential of EEG to investigate brain activity triggered by umami stimuli.

The Role of ATP and Purinergic Receptors in Taste Signaling.

This review summarizes our understanding of ATP signaling in taste and describes new directions for research. ATP meets all requisite criteria to be considered a neurotransmitter: (1) presence in taste cells, as in all cells; (2) release upon appropriate taste stimulation; (3) binding to cognate purinergic receptors P2X2 and P2X3 on gustatory afferent neurons, and (4) after release, enzymatic degradation to adenosine and other nucleotides by the ectonucleotidase, NTPDase2, expressed on the Type I, glial-like cells in the taste bud. Importantly, double knockout of P2X2 and P2X3 or pharmacological inhibition of P2X3 abolishes transmission of all taste qualities. In Type II taste cells (those that respond to sweet, bitter, or umami stimuli), ATP is released non-vesicularly by a large conductance ion channel composed of CALHM1 and CALHM3, which form a so-called channel synapse at areas of contact with afferent taste nerve fibers. Although ATP release has been detected only from Type II cells, it is also required for the transmission of salty and sour stimuli, which are mediated primarily by the Type III taste cells. The source of the ATP required for Type III cell signaling to afferent fibers is still unclear and is a focus for future experiments. The ionotropic purinergic receptor, P2X3, is widely expressed on many sensory afferents and has been a therapeutic target for treating chronic cough and pain. However, its requirement for taste signaling has complicated efforts at treatment since patients given P2X3 antagonists report substantial disturbances of taste and become non-compliant.

Alteration, Reduction and Taste Loss: Main Causes and Potential Implications on Dietary Habits.

Our sense of taste arises from the sensory information generated after compounds in the oral cavity and oropharynx activate taste receptor cells situated on taste buds. This produces the perception of sweet, bitter, salty, sour, or umami stimuli, depending on the chemical nature of the tastant. Taste impairments (dysgeusia) are alterations of this normal gustatory functioning that may result in complete taste losses (ageusia), partial reductions (hypogeusia), or over-acuteness of the sense of taste (hypergeusia). Taste impairments are not life-threatening conditions, but they can cause sufficient discomfort and lead to appetite loss and changes in eating habits, with possible effects on health. Determinants of such alterations are multiple and consist of both genetic and environmental factors, including aging, exposure to chemicals, drugs, trauma, high alcohol consumption, cigarette smoking, poor oral health, malnutrition, and viral upper respiratory infections including influenza. Disturbances or loss of smell, taste, and chemesthesis have also emerged as predominant neurological symptoms of infection by the recent Coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus strain 2 (SARS-CoV-2), as well as by previous both endemic and pandemic coronaviruses such as Middle East Respiratory Syndrome Coronavirus (MERS-CoV) and SARS-CoV. This review is focused on the main causes of alteration, reduction, and loss of taste and their potential repercussion on dietary habits and health, with a special focus on the recently developed hypotheses regarding the mechanisms through which SARS-CoV-2 might alter taste perception.

A subset of broadly responsive Type III taste cells contribute to the detection of bitter, sweet and umami stimuli.

Taste receptor cells use multiple signaling pathways to detect chemicals in potential food items. These cells are functionally grouped into different types: Type I cells act as support cells and have glial-like properties; Type II cells detect bitter, sweet, and umami taste stimuli; and Type III cells detect sour and salty stimuli. We have identified a new population of taste cells that are broadly tuned to multiple taste stimuli including bitter, sweet, sour, and umami. The goal of this study was to characterize these broadly responsive (BR) taste cells. We used an IP3R3-KO mouse (does not release calcium (Ca2+) from internal stores in Type II cells when stimulated with bitter, sweet, or umami stimuli) to characterize the BR cells without any potentially confounding input from Type II cells. Using live cell Ca2+ imaging in isolated taste cells from the IP3R3-KO mouse, we found that BR cells are a subset of Type III cells that respond to sour stimuli but also use a PLCβ signaling pathway to respond to bitter, sweet, and umami stimuli. Unlike Type II cells, individual BR cells are broadly tuned and respond to multiple stimuli across different taste modalities. Live cell imaging in a PLCβ3-KO mouse confirmed that BR cells use this signaling pathway to respond to bitter, sweet, and umami stimuli. Short term behavioral assays revealed that BR cells make significant contributions to taste driven behaviors and found that loss of either PLCβ3 in BR cells or IP3R3 in Type II cells caused similar behavioral deficits to bitter, sweet, and umami stimuli. Analysis of c-Fos activity in the nucleus of the solitary tract (NTS) also demonstrated that functional Type II and BR cells are required for normal stimulus induced expression.

Electrophysiological responses to sugars and amino acids in the nucleus of the solitary tract of type 1 taste receptor double-knockout mice.

Strong evidence supports a major role for heterodimers of the type 1 taste receptor (T1R) family in the taste transduction of sugars (T1R2+T1R3) and amino acids (T1R1+T1R3), but there are also neural and behavioral data supporting T1R-independent mechanisms. Most neural evidence for alternate mechanisms comes from whole nerve recordings in mice with deletion of a single T1R family member, limiting conclusions about the functional significance and T1R independence of the remaining responses. To clarify these issues, we recorded single-unit taste responses from the nucleus of the solitary tract in T1R double-knockout (double-KO) mice lacking functional T1R1+T1R3 [KO1+3] or T1R2+T1R3 [KO2+3] receptors and their wild-type background strains [WT; C57BL/6J (B6), 129X1/SvJ (S129)]. In both double-KO strains, responses to sugars and a moderate concentration of an monosodium glutamate + amiloride + inosine 5'-monophosphate cocktail (0.1 M, i.e., umami) were profoundly depressed, whereas a panel of 0.6 M amino acids were mostly unaffected. Strikingly, in contrast to WT mice, no double-KO neurons responded selectively to sugars and umami, precluding segregation of this group of stimuli from those representing other taste qualities in a multidimensional scaling analysis. Nevertheless, residual sugar responses, mainly elicited by monosaccharides, persisted as small "sideband" responses in double-KOs. Thus other receptors may convey limited information about sugars to the central nervous system, but T1Rs appear critical for coding the distinct perceptual features of sugar and umami stimuli. The persistence of amino acid responses supports previous proposals of alternate receptors, but because these stimuli affected multiple neuron types, further investigations are necessary.NEW & NOTEWORTHY The type 1 taste receptor (T1R) family is crucial for transducing sugars and amino acids, but there is evidence for T1R-independent mechanisms. In this study, single-unit recordings from the nucleus of the solitary tract in T1R double-knockout mice lacking T1R1+T1R3 or T1R2+T1R3 receptors revealed greatly reduced umami synergism and sugar responses. Nevertheless, residual sugar responses persisted, mainly elicited by monosaccharides and evident as "sidebands" in neurons activated more vigorously by other qualities.

Function, Innervation, and Neurotransmitter Signaling in Mice Lacking Type-II Taste Cells.

The Skn-1a transcription factor (Pou2f3) is required for Type II taste cell differentiation in taste buds. Taste buds in Skn-1a-/- mice lack Type II taste cells but have a concomitant expansion of Type III cells, providing an ideal model to determine the relative role of taste cell types in response specificity. We confirmed that chorda tympani responses to sweet, bitter, and umami stimuli were greatly reduced in the knock-outs (KOs) compared with wild-type (WT) littermates. Skn-1a-/- mice also had reductions to NaCl that were partially amiloride-insensitive, suggesting that both Type II and Type III cells contribute to amiloride-insensitive salt detection in anterior tongue. We also confirmed that responses to sour stimuli are equivalent in the KOs, despite the large increase in the number of Type III taste cells. To examine their innervation, we crossed the Htr3a-GFP (5-HT3A-GFP) reporter mouse with the Skn-1a-/- mice and examined geniculate ganglion neurons for GFP expression and responses to 5-HT. We found no change in the number of 5-HT3A-expressing neurons with KO of Skn-1a. Calcium imaging showed that only 5-HT3A-expressing neurons respond to exogenous 5-HT, while most neurons respond to ATP, similar to WT mice. Interestingly, despite loss of all Type II cells, the P2X3 antagonist AF353 blocked all chorda tympani responses. These data collectively raise questions pertaining the source of ATP signaling in the absence of Type II taste cells and whether the additional Type III cells are innervated by fibers that would have normally innervated Type II cells.

Metabolic control via nutrient-sensing mechanisms: role of taste receptors and the gut-brain neuroendocrine axis.

Nutrient sensing plays an important role in ensuring that appropriate digestive or hormonal responses are elicited following the ingestion of fuel substrates. Mechanisms of nutrient sensing in the oral cavity have been fairly well characterized and involve lingual taste receptors. These include heterodimers of G protein-coupled receptors (GPCRs) of the taste receptor type 1 (T1R) family for sensing sweet (T1R2-T1R3) and umami (T1R1-T1R3) stimuli, the T2R family for sensing bitter stimuli, and ion channels for conferring sour and salty tastes. In recent years, several studies have revealed the existence of additional nutrient-sensing mechanisms along the gastrointestinal tract. Glucose sensing is achieved by the T1R2-T1R3 heterodimer on enteroendocrine cells, which plays a role in triggering the secretion of incretin hormones for improved glycemic and lipemic control. Protein hydrolysates are detected by Ca2+-sensing receptor, the T1R1-T1R3 heterodimer, and G protein-coupled receptor 92/93 (GPR92/93), which leads to the release of the gut-derived satiety factor cholecystokinin. Furthermore, several GPCRs have been implicated in fatty acid sensing: GPR40 and GPR120 respond to medium- and long-chain fatty acids, GPR41 and GPR43 to short-chain fatty acids, and GPR119 to endogenous lipid derivatives. Aside from the recognition of fuel substrates, both the oral cavity and the gastrointestinal tract also possess T2R-mediated mechanisms of recognizing nonnutrients such as environmental contaminants, bacterial toxins, and secondary plant metabolites that evoke a bitter taste. These gastrointestinal sensing mechanisms result in the transmission of neuronal signals to the brain through the release of gastrointestinal hormones that act on vagal and enteric afferents to modulate the physiological response to nutrients, particularly satiety and energy homeostasis. Modulating these orally accessible nutrient-sensing pathways using particular foods, dietary supplements, or pharmaceutical compounds may have therapeutic potential for treating obesity and metabolic diseases.

Prolonged Exposure to Monosodium Glutamate in Healthy Young Adults Decreases Perceived Umami Taste and Diminishes Appetite for Savory Foods

Research suggests that increased consumption of sweet, salt, or fat is associated with diminished perceived taste intensity and shifted preferences for the respective stimulus. It is unknown whether a similar effect occurs with the consumption of umami. The aim of the study was to investigate the influence of habitual exposure to umami stimuli on umami taste perception, hedonics, and satiety. Fifty-eight healthy men (n=16) and women (n=42) participated in a parallel-group, randomized controlled study. The normal-weight [mean ± SD body mass index (kg/m2): 21.8±2.2] group of young adults (mean ± SD age: 22.7±6.2 y) consumed vegetable broth daily for 4 wk. The broth for the treatment group (n=28) was supplemented with 3.8 g monosodium glutamate (MSG), whereas the control group (n=30) consumed a sodium-matched broth without MSG. Perceived umami taste intensity and discrimination in MSG solutions; liking, wanting, and preference of a variety of umami-rich foods; satiation and satiety from an ad libitum meal; and anthropometric measures were evaluated at baseline and at week 4. General linear models assessed the effect of treatment on change from baseline for all outcomes and tested for effect modification of sex. Relative to controls, increased consumption of MSG for 4 wk diminished umami taste in women (8.4 units on generalized Labeled Magnitude Scale; 95% CI: -13.8, -3.1 units; P=0.013). The desire for and intake of savory foods decreased after MSG treatment in both sexes with an ad libitum meal (desire: -7.7 units; 95% CI: -13.7, -1.7 units; P=0.04; intake: -36 g; 95% CI: -91, 19 g; P=0.04). Our results highlight that a month-long diet high in umami stimuli attenuates perceived umami taste and appetite for savory foods in a young, healthy population. Our findings contribute to the understanding of food choice, a factor in the development and maintenance of obesity, as well as the etiology of protein-related health conditions such as osteoporosis and kidney disease. This study is registered at www.clinicaltrials.gov as NCT03010930.

Gli3 is a negative regulator of Tas1r3-expressing taste cells.

Mouse taste receptor cells survive from 3–24 days, necessitating their regeneration throughout adulthood. In anterior tongue, sonic hedgehog (SHH), released by a subpopulation of basal taste cells, regulates transcription factors Gli2 and Gli3 in stem cells to control taste cell regeneration. Using single-cell RNA-Seq we found that Gli3 is highly expressed in Tas1r3-expressing taste receptor cells and Lgr5+ taste stem cells in posterior tongue. By PCR and immunohistochemistry we found that Gli3 was expressed in taste buds in all taste fields. Conditional knockout mice lacking Gli3 in the posterior tongue (Gli3CKO) had larger taste buds containing more taste cells than did control wild-type (Gli3WT) mice. In comparison to wild-type mice, Gli3CKO mice had more Lgr5+ and Tas1r3+ cells, but fewer type III cells. Similar changes were observed ex vivo in Gli3CKO taste organoids cultured from Lgr5+ taste stem cells. Further, the expression of several taste marker and Gli3 target genes was altered in Gli3CKO mice and/or organoids. Mirroring these changes, Gli3CKO mice had increased lick responses to sweet and umami stimuli, decreased lick responses to bitter and sour taste stimuli, and increased glossopharyngeal taste nerve responses to sweet and bitter compounds. Our results indicate that Gli3 is a suppressor of stem cell proliferation that affects the number and function of mature taste cells, especially Tas1r3+ cells, in adult posterior tongue. Our findings shed light on the role of the Shh pathway in adult taste cell regeneration and may help devise strategies for treating taste distortions from chemotherapy and aging.

TRPM4 and TRPM5 are both required for normal signaling in taste receptor cells

Peripheral taste receptor cells use multiple signaling pathways to transduce taste stimuli into output signals that are sent to the brain. Transient receptor potential melastatin 5 (TRPM5), a sodium-selective TRP channel, functions as a common downstream component in sweet, bitter, and umami signaling pathways. In the absence of TRPM5, mice have a reduced, but not abolished, ability to detect stimuli, suggesting that a TRPM5-independent pathway also contributes to these signals. Here, we identify a critical role for the sodium-selective TRP channel TRPM4 in taste transduction. Using live cell imaging and behavioral studies in KO mice, we show that TRPM4 and TRPM5 are both involved in taste-evoked signaling. Loss of either channel significantly impairs taste, and loss of both channels completely abolishes the ability to detect bitter, sweet, or umami stimuli. Thus, both TRPM4 and TRPM5 are required for transduction of taste stimuli.

Biophysical and functional characterization of the N-terminal domain of the cat T1R1 umami taste receptor expressed in Escherichia coli.

Umami taste perception is mediated by the heterodimeric G-protein coupled receptors (GPCRs), formed by the assembly of T1R1 and T1R3 subunits. T1R1 and T1R3 subunits are class C GPCRs whose members share common structural homologies including a long N-terminal domain (NTD) linked to a seven transmembrane domain by a short cysteine-rich region. The NTD of the T1R1 subunit contains the primary binding site for umami stimuli, such as L-glutamate (L-Glu) for humans. Inosine-5’-monophosphate (IMP) binds at a location close to the opening of the T1R1-NTD “flytrap”, thus creating the observed synergistic response between L-Glu and IMP. T1R1/T1R3 binding studies have revealed species-dependent differences. While human T1R1/T1R3 is activated specifically by L-Glu, the T1R1/T1R3 in other species is a broadly tuned receptor, sensitive to a range of L-amino acids. Because domestic cats are obligate carnivores, they display strong preferences for some specific amino acids. To better understand the structural basis of umami stimuli recognition by non-human taste receptors, we measured the binding of selected amino acids to cat T1R1/T1R3 (cT1R1/cT1R3) umami taste receptor. For this purpose, we expressed cT1R1-NTD in bacteria as inclusion bodies. After purification, refolding of the protein was achieved. Circular dichroism spectroscopic studies revealed that cT1R1-NTD was well renatured with evidence of secondary structures. Using size-exclusion chromatography coupled to light scattering, we found that the cT1R1-NTD behaves as a monomer. Ligand binding quantified by intrinsic tryptophan fluorescence showed that cT1R1-NTD is capable of binding L-amino acids with Kd values in the micromolar range. We demonstrated that IMP potentiates L-amino acid binding onto renatured cT1R1-NTD. Interestingly, our results revealed that IMP binds the extracellular domain in the absence of L-amino acids. Thus, this study demonstrates that the feasibility to produce milligram quantities of cT1R1-NTD for functional and structural studies.

Temperature Influences Chorda Tympani Nerve Responses to Sweet, Salty, Sour, Umami, and Bitter Stimuli in Mice.

Temperature profoundly affects the perceived intensity of taste, yet we know little of the extent of temperature's effect on taste in the peripheral nervous system. Accordingly, we investigated the influence of temperature from 23 °C to 43 °C in 4 °C intervals on the integrated responses of the chorda tympani (CT) nerve to a large series of chemical stimuli representing sweet, salty, sour, bitter, and umami tastes in C57BL/J6 mice. We also measured neural responses to NaCl, Na-gluconate, Na-acetate, Na-sulfate, and MSG with and without 5 µM benzamil, an epithelial sodium channel (ENaC) antagonist, to assess the influence of temperature on ENaC-dependent and ENaC-independent response components. Our results showed that for most stimuli (0.5M sucrose, glucose, fructose, and maltose; 0.02M saccharin and sucralose; 0.5M NaCl, Na-gluconate, Na-acetate, Na-sulfate, KCl, K-gluconate, K-acetate, and K-sulfate; 0.05M citric acid, acetic acid, and HCl; 0.1M MSG and 0.05M quinine hydrochloride: QHCl), CT response magnitudes were maximal between 35 °C and 39 °C and progressively smaller at cooler or warmer temperatures. In contrast, the weakest responses to NH 4 Cl, (NH 4 ) 2 SO4, and K-sulfate were at the lowest temperature, with response magnitude increasing monotonically with increasing temperature, while the largest responses to acetic acid were at the lowest temperature, with response magnitude decreasing with increasing temperature. The response to sweet and umami stimuli across temperatures were similar reflecting the involvement of TRPM5 activity, in contrast to bitter stimuli, which were weakly affected by temperature. Temperature-modulated responses to salts and acids most likely operate through mechanisms independent of ENaC and TRPM5.

Cerebral processing of umami: A pilot study on the effects of familiarity

AimThe identification of umami taste among people is extremely variable. Based on functional magnetic resonance imaging (fMRI) the aim of this study was to investigate changes of brain activation in participants before and after they were familiarized with this peculiar taste. Material and methodA total of 10 healthy, right-handed subjects (7 women, mean age 25 years) participated in this study. A computer-controlled gustometer was used to deliver the umami stimuli at supra-threshold concentrations. After the first session of fMRI experiments, participants went through two weeks of controlled exposure to umami taste, before the second session of fMRI experimentation. ResultsResults from psychophysical assessment showed that umami became more familiar (p<0.001) among the participants after the gustatory exposure. No significant differences for pleasantness and intensity were observed before and after umami training. FMRI data showed that a broader central-nervous network was activated before “umami training” as compared to imaging after “umami training”. Significant activation was found in the primary and high level sensory specific gustatory area (insula and anterior cingulate cortex) before training, whereas, significant activation was observed in memory retrieval areas (parahippocampal gyrus) after training. ConclusionThe main finding of the present study suggests that repeated exposure to umami taste over a relatively short period of time does not produce an increased response at the level of taste primary and secondary areas, but that increased familiarity with umami leads to an increased activation of the parahippocampal gyrus.

How taste works: cells, receptors and gustatory perception.

The sensitivity of taste in mammals varies due to quantitative and qualitative differences in the structure of the taste perception organs. Gustatory perception is made possible by the peripheral chemosensory organs, i.e., the taste buds, which are distributed in the epithelium of the taste papillae of the palate, tongue, epiglottis, throat and larynx. Each taste bud consists of a community of ~100 cells that process and integrate taste information with metabolic needs. Mammalian taste buds are contained in circumvallate, fungiform and foliate papillae and react to sweet, salty, sour, bitter and umami stimuli. The sensitivity of the taste buds for individual taste stimuli varies extensively and depends on the type of papillae and the part of the oral cavity in which they are located. There are at least three different cell types found in mammalian taste buds: type I cells, receptor (type II) cells and presynaptic (type III) cells. This review focuses on the biophysiological mechanisms of action of the various taste stimuli in humans. Currently, the best-characterized proteins are the receptors (GPCR). In addition, the activation of bitter, sweet and umami tastes are relatively well known, but the activation of salty and sour tastes has yet to be clearly explained.

Sodium aspartate as a specific enhancer of salty taste perception-sodium aspartate is a possible candidate to decrease excessive intake of dietary salt.

The excessive intake of dietary salt is a global issue in health. Attempts have been made to address this issue, including the development of salt substitutes. Yet, none of these substances are currently in wide use, because of their weak saltiness. The purpose of this study was to assess the effects of sodium aspartate (Asp-Na) on salty taste perception using the bullfrog glossopharyngeal nerve response and human sensory tests. When added to the mixture of NaCl and KCl, Asp-Na significantly enhanced the glossopharyngeal nerve response to the mixture by 1.6-fold compared to control. Asp-Na did not enhance the response to NaCl, nor did Asp-Na enhance the response to sour, bitter, or umami stimuli. The optimal concentration for Asp-Na to enhance the salt mixture was 1.7mM. The largest enhancement was induced when NaCl and KCl were mixed at equimolar concentrations. Asp-Na significantly suppressed the glossopharyngeal nerve response to quinine hydrochloride, which suggests that bitterness of KCl is suppressed by Asp-Na. The salty taste enhancing effect of Asp-Na was also confirmed with human sensory tests. The present results suggested that the mixture of NaCl and KCl containing Asp-Na can be used as a salt substitute. In addition to demonstrating that Asp-Na enhanced salt taste responses in an experimental animal and human, our findings provide clues to identify the elusive salty taste receptors.

Umami evaluation in taste epithelium on microelectrode array by extracellular electrophysiological recording

Umami is one of the basic tastes along with sweet, bitter, sour and salty. It is often elicited by amino acids and can provide a palatable flavor for food. With taste epithelium as the sensing element, microelectrodes can be used to evaluate umami taste by biological responses of the tissue. The electrophysiological activities to umami stimuli are measured with a 60-channel microelectrode array (MEA). Local field potential (LFP) recorded by a MEA system showed different temporal characteristics respectively with l-glutamic acid (l-Glu), l-aspartic acid (l-Asp), l-monosodium glutamate (l-MSG) and l-monosodium aspartate (l-MSA), while remarkable differences were observed between amino acids and their sodium salts. Wealso found that a dose-dependent behavior in the increasing concentrations of umami stimulations and a synergistic enhancement between amino acids and purine nucleotides can be detected. The investigation of this evaluation for umami represents a promising approach for distinguishing and evaluating umami tastants.