Taste Buds and Gustatory Transduction: A Functional Perspective

Author(s):  
Alan C. Spector ◽  
Susan P. Travers

Everything a person swallows must pass a final chemical analysis by the sensory systems of the mouth; of these, the gustatory system is cardinal. Gustation can be heuristically divided into three basic domains of function: sensory-discriminative (quality and intensity), motivational/affective (promote or deter ingestion), and physiological (e.g., salivation and insulin release). The signals from the taste buds, transmitted to the brain through the sensory branches of cranial nerves VII (facial), IX (glossopharyngeal), and X (vagal), subserve these primary functions. Taste buds are collections of 50–100 cells that are distributed in various fields in the tongue, soft palate, and throat. There are three types of cells that have been identified in taste buds based on their morphological and cytochemical expression profiles. Type II cells express specialized G-protein-coupled receptors (GPCR or GPR) on their apical membranes, which protrude through a break in the oral epithelial lining called the taste pore, that are responsible for the sensing of sweeteners (via the taste type 1 receptor (T1R) 2 + T1R3), amino acids (via the T1R1+T1R3), and bitter ligands (via the taste type 2 receptors (T2Rs)). Type III cells are critical for the sensing of acids via the otopetrin-1 (Otop-1) ion channel. The sensing of sodium, in at least rodents, occurs through the epithelial sodium channel (ENaC), but the exact composition of this channel and the type of taste cell type in which the functional version resides remains unclear. It is controversial whether Type I cells, which have been characterized as glial-like, are involved in sodium transduction or play any taste signaling role. For the most part, receptors for different stimulus classes (e.g., sugars vs. bitter ligands) are not co-expressed, providing significant early functionally related segregation of signals. There remains a persistent search for yet to be identified receptors that may contribute to some functions associated with stimuli representing the so-called basic taste qualities—sweet, salty, sour, bitter, and umami—as well as unconventional stimuli such as fatty acids (in addition to cluster of differentiation-36 (CD-36), GPR40, and GPR120) and maltodextrins. The primary neurotransmitter in taste receptor cells is ATP, which is released through a voltage-gated heteromeric channel consisting of the calcium homeostasis modulator 1 and 3 (CALHM1/3) and binds with P2X2/X3 receptors on apposed afferent fibers. Serotonin released from Type III cells has been implicated as an additional neurotransmitter, binding with HT3a receptors, and possibly playing a role in acid taste (which is sour to humans). Taste bud cells undergo complete turnover about every two weeks. Although there remains much to be understood about the operations of the taste bud, perhaps the one very clear principle that emerges is that the organization of signals transmitted to the brain is not random and arbitrary to be decoded by complex algorithms in the circuits of the central gustatory system. Rather, the transmission of taste information from the periphery is highly ordered.

1992 ◽  
Vol 3 (4) ◽  
pp. 371-393 ◽  
Author(s):  
Marion E. Frank ◽  
Thomas P. Hettinger ◽  
April E. Mott

The sense of taste is an oral chemical sense in mammals that is involved in the choice of foods. Initial transduction of taste stimuli occurs in taste buds, which are distributed in four discrete fields in the oral cavity. Medications can affect the taste buds and ion channels in taste-bud cell membranes involved in stimulus transduction. The sense of taste gradually declines with aging, with bitter taste most affected. Neural circuits that mediate taste in primates include cranial nerves VII, IX, and X, the solitary nucleus in the brain stem, the ventroposteromedial nucleus of the thalamus, and the insular-opercular cortex. The central taste pathways process taste information about sweet, salty, sour, and bitter stimuli serially and in parallel. Medications associated with "metallic" dysgeusia and taste losses affect the taste system via unknown mechanisms.


Author(s):  
Sunao Fujimoto ◽  
Raymond G. Murray ◽  
Assia Murray

Taste bud cells in circumvallate papillae of rabbit have been classified into three groups: dark cells; light cells; and type III cells. Unilateral section of the 9th nerve distal to the petrosal ganglion was performed in 18 animals, and changes of each cell type in the denervated buds were observed from 6 hours to 10 days after the operation.Degeneration of nerves is evident at 12 hours (Fig. 1) and by 2 days, nerves are completely lacking in the buds. Invasion by leucocytes into the buds is remarkable from 6 to 12 hours but then decreases. Their extrusion through the pore is seen. Shrinkage and disturbance in arrangement of cells in the buds can be seen at 2 days. Degenerated buds consisting of a few irregular cells and remnants of degenerated cells are present at 4 days, but buds apparently normal except for the loss of nerve elements are still present at 6 days.


2020 ◽  
Vol 45 (4) ◽  
pp. 261-273
Author(s):  
Takahiro Ogata ◽  
Yoshitaka Ohtubo

Abstract A mouse single taste bud contains 10–100 taste bud cells (TBCs) in which the elongated TBCs are classified into 3 cell types (types I–III) equipped with different taste receptors. Accordingly, differences in the cell numbers and ratios of respective cell types per taste bud may affect taste-nerve responsiveness. Here, we examined the numbers of each immunoreactive cell for the type II (sweet, bitter, or umami receptor cells) and type III (sour and/or salt receptor cells) markers per taste bud in the circumvallate and foliate papillae and compared these numerical features of TBCs per taste bud to those in fungiform papilla and soft palate, which we previously reported. In circumvallate and foliate taste buds, the numbers of TBCs and immunoreactive cells per taste bud increased as a linear function of the maximal cross-sectional taste bud area. Type II cells made up approximately 25% of TBCs irrespective of the regions from which the TBCs arose. In contrast, type III cells in circumvallate and foliate taste buds made up approximately 11% of TBCs, which represented almost 2 times higher than what was observed in the fungiform and soft palate taste buds. The densities (number of immunoreactive cells per taste bud divided by the maximal cross-sectional area of the taste bud) of types II and III cells per taste bud are significantly higher in the circumvallate papillae than in the other regions. The effects of these region-dependent differences on the taste response of the taste bud are discussed.


2020 ◽  
Vol 45 (7) ◽  
pp. 533-539
Author(s):  
Aurelie Vandenbeuch ◽  
Courtney E Wilson ◽  
Sue C Kinnamon

Abstract Studies have suggested that communication between taste cells shapes the gustatory signal before transmission to the brain. To further explore the possibility of intragemmal signal modulation, we adopted an optogenetic approach to stimulate sour-sensitive (Type III) taste cells using mice expressing Cre recombinase under a specific Type III cell promoter, Pkd2l1 (polycystic kidney disease-2-like 1), crossed with mice expressing Cre-dependent channelrhodopsin (ChR2). The application of blue light onto the tongue allowed for the specific stimulation of Type III cells and circumvented the nonspecific effects of chemical stimulation. To understand whether taste modality information is preprocessed in the taste bud before transmission to the sensory nerves, we recorded chorda tympani nerve activity during light and/or chemical tastant application to the tongue. To assess intragemmal modulation, we compared nerve responses to various tastants with or without concurrent light-induced activation of the Type III cells. Our results show that light significantly decreased taste responses to sweet, bitter, salty, and acidic stimuli. On the contrary, the light response was not consistently affected by sweet or bitter stimuli, suggesting that activation of Type II cells does not affect nerve responses to stimuli that activate Type III cells.


2019 ◽  
Author(s):  
Debarghya Dutta Banik ◽  
Eric D. Benfey ◽  
Laura E. Martin ◽  
Kristen E. Kay ◽  
Gregory C. Loney ◽  
...  

ABSTRACTTaste 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 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 PLCβ3 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 a PLCβ3 signaling pathway to generate Ca2+ signals to bitter, sweet and umami stimuli. Analysis of c-Fos activity in the nucleus of the solitary tract (NTS) and short term behavioral assays revealed that BR cells make significant contributions to taste.


2021 ◽  
Vol 15 ◽  
Author(s):  
Elena von Molitor ◽  
Katja Riedel ◽  
Michael Krohn ◽  
Mathias Hafner ◽  
Rüdiger Rudolf ◽  
...  

Sweetness is the preferred taste of humans and many animals, likely because sugars are a primary source of energy. In many mammals, sweet compounds are sensed in the tongue by the gustatory organ, the taste buds. Here, a group of taste bud cells expresses a canonical sweet taste receptor, whose activation induces Ca2+ rise, cell depolarization and ATP release to communicate with afferent gustatory nerves. The discovery of the sweet taste receptor, 20 years ago, was a milestone in the understanding of sweet signal transduction and is described here from a historical perspective. Our review briefly summarizes the major findings of the canonical sweet taste pathway, and then focuses on molecular details, about the related downstream signaling, that are still elusive or have been neglected. In this context, we discuss evidence supporting the existence of an alternative pathway, independent of the sweet taste receptor, to sense sugars and its proposed role in glucose homeostasis. Further, given that sweet taste receptor expression has been reported in many other organs, the physiological role of these extraoral receptors is addressed. Finally, and along these lines, we expand on the multiple direct and indirect effects of sugars on the brain. In summary, the review tries to stimulate a comprehensive understanding of how sweet compounds signal to the brain upon taste bud cells activation, and how this gustatory process is integrated with gastro-intestinal sugar sensing to create a hedonic and metabolic representation of sugars, which finally drives our behavior. Understanding of this is indeed a crucial step in developing new strategies to prevent obesity and associated diseases.


1997 ◽  
Vol 3 (1) ◽  
pp. 53-69 ◽  
Author(s):  
Bert Ph.M. Menco ◽  
Maya P. Yankova ◽  
Sidney A. Simon

Abstract: We have explored freeze-substitution combined with low-temperature embedding in rat taste buds for postembedding immunocytochemistry. A major difference in taste bud cells that were rapidly frozen without prior chemical fixation and those that were fixed and cryoprotected before freezing was that electron-dense core granules were virtually absent. The antibodies used in these initial studies were directed against calcitonin gene-related peptide (CGRP), a peptide commonly found in nociceptive neurons; the α-subunits of two G-proteins involved in bitter and sweet taste transduction; and choline acetyl transferase (ChAT), an enzyme involved in the synthesis of acetylcholine. Anti-CGRP immunolabeled a subpopulation of unmyelinated perigemmal neurons; anti-Gqα labeled a larger subpopulation of these neurons and the microvilli of cells that were most likely from Type II vallate taste buds. α-Gustducin was found in cytoplasm of Type II and/or III cells and probably in microvilli of Type I cells of vallate taste buds. The best labeling results were obtained with anti-ChAT, which stained microvilli and lateral membranes of some Type II vallate taste bud cells, and the cytoplasm of some other Type II and/or III vallate cells. In addition, anti-ChAT labeled electron-opaque materials inside taste bud pores of vallate papillae, but, under the same conditions, not granules of Type I cells or most of the vesicles in von Ebner's glands. These data suggest that we can not assume a priori that the contents of the electron-dense core granules of Type I cells, or even of those of von Ebner's glands, contain the precursors of the taste bud pore–dense substances.


Development ◽  
1996 ◽  
Vol 122 (4) ◽  
pp. 1103-1111 ◽  
Author(s):  
L.A. Barlow ◽  
C.B. Chien ◽  
R.G. Northcutt

It has been hypothesized that taste buds are induced by contact with developing cranial nerve fibers late in embryonic development, since descriptive studies indicate that during embryonic development taste cell differentiation occurs concomitantly with or slightly following the advent of innervation. However, experimental evidence delineating the role of innervation in taste bud development is sparse and equivocal. Using two complementary experimental approaches, we demonstrate that taste cells differentiate fully in the complete absence of innervation. When the presumptive oropharyngeal region was taken from a donor axolotl embryo, prior to its innervation and development of taste buds, and grafted ectopically on to the trunk of a host embryo, the graft developed well-differentiated taste buds. Although grafts were invaded by branches of local spinal nerves, these neurites were rarely found near ectopic taste cells. When the oropharyngeal region was raised in culture, numerous taste buds were generated in the complete absence of neural elements. Taste buds in grafts and in explants were identical to those found in situ both in terms of their morphology and their expression of calretinin and serotonin immunoreactivity. Our findings indicate that innervation is not necessary for complete differentiation of taste receptor cells. We propose that taste buds are either induced in response to signals from other tissues, such as the neural crest, or arise independently through intrinsic patterning of the local epithelium.


Author(s):  
Stephen D. Roper ◽  
Nirupa Chaudhari

Taste buds are the sensory end organs of the gustatory system. Thousands of these tiny sensory structures are embedded throughout the lingual epithelium and palate. As well-defined anatomical structures, taste buds can provide valuable insight into microcircuit organization. Information transmitted by taste buds to the brain results in conscious perceptions of taste—sweet, sour, salty, bitter, umami, and perhaps fat and others, but they also generate signals that initiate physiological reflexes such as a rapid burst of insulin secretion from the pancreatic islets to prepare the digestive tract for food. These responses are termed cephalic phase reflexes. This chapter presents an overview of how cell-cell communication and synaptic transmission within taste buds might underlie information processing in these sensory end organs, and perhaps also sheds light on the problem of taste coding, at least at its initial stages in the periphery.


1996 ◽  
Vol 107 (4) ◽  
pp. 545-554 ◽  
Author(s):  
R E Doolin ◽  
T A Gilbertson

The role of amiloride-sensitive Na+ channels (ASSCs) in the transduction of salty taste stimuli in rat fungiform taste buds has been well established. Evidence for the involvement of ASSCs in salt transduction in circumvallate and foliate taste buds is, at best, contradictory. In an attempt to resolve this apparent controversy, we have begun to look for functional ASSCs in taste buds isolated from fungiform, foliate, and circumvallate papillae of male Sprague-Dawley rats. By use of a combination of whole-cell and nystatin-perforated patch-clamp recording, cells within the taste bud that exhibited voltage-dependent currents, reflective of taste receptor cells (TRCs), were subsequently tested for amiloride sensitivity. TRCs were held at -70 mV, and steady-state current and input resistance were monitored during superfusion of Na(+)-free saline and salines containing amiloride (0.1 microM to 1 mM). Greater than 90% of all TRCs from each of the papillae responded to Na+ replacement with a decrease in current and an increase in input resistance, reflective of a reduction in electrogenic Na+ movement into the cell. ASSCs were found in two thirds of fungiform and in one third of foliate TRCs, whereas none of the circumvallate TRCs was amiloride sensitive. These findings indicate that the mechanism for Na+ influx differs among taste bud types. All amiloride-sensitive currents had apparent inhibition constants in the submicromolar range. These results agree with afferent nerve recordings and raise the possibility that the extensive labeling of the ASSC protein and mRNA in the circumvallate papillae may reflect a pool of nonfunctional channels or a pool of channels that lacks sensitivity to amiloride.


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