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PubMed2003

Sour-taste tolerance in four species of nonhuman primates.

The taste of most fruits is characterized by a mixture of sensations termed sweet and sour by humans, and the food selection behavior of primates suggests that they may use the relative salience of sweetness and sourness to assess palatability of potential food items. Therefore, taste responses of six squirrel monkeys, five pigtail macaques, four olive baboons, and four spider monkeys to sweet-sour taste mixtures were assessed in two-bottle preference tests of brief duration (2 min). Monkeys were given the choice between a reference solution of 50 mM sucrose and mixtures containing 10, 30, or 50 mM citric acid plus 10, 20, 50, 100, 200, 400, 800, or 1000 mM sucrose. We found that the four species differed markedly in their acceptance of physiological concentrations of sour-tasting citric acid. Whereas olive baboons showed the highest degree of sour-taste tolerance and actually preferred most of the sweet-sour taste mixtures over sweet-tasting reference solutions, squirrel monkeys showed the lowest degree of sour-taste tolerance and rejected most of the sweet-sour taste mixtures even when they contained considerably more sucrose than the reference solutions. Additional tests demonstrated that the preference for sweet-sour taste mixtures was not based on masking effects. Rather, the animals perceived both the sweetness and the sourness of the taste mixtures and made a trade-off between the attractive and aversive properties of the two taste qualities. The results of this study suggest that the proximate reason for the marked differences in acceptance of sweet-sour taste mixtures are differences among species in the hedonic evaluation of the sour taste of citric acid. Possible ultimate reasons, which do not necessarily exclude, but may complement each other, include evolutionary adaptation to dietary specialization, avoidance of competition pressure, and phylogenetic relatedness.

Animals↗
PubMed1996

The distribution and origin of keratin 20-containing taste buds in rat and human.

Sections of tissues containing lingual and extra-lingual taste buds were evaluated with monoclonal antibodies against cytokeratins. In the caudal third of the rat's tongue, keratin 20 immunoreactivity was restricted to taste buds, whereas keratins 7, 8, 18, and 19 were expressed in vallate and foliate taste buds and in cells of salivary ducts that merge with these taste epithelia. Hence, antibodies against keratin 20 most clearly distinguished differentiated taste cells from all other cells. In rat epiglottis, taste buds and isolated bipolar cells were keratin-20-positive. In rat nasopalatine papilla and palate, antibodies against keratin 20 identified Merkel cells, none of which was near to the keratin-20-negative taste buds. Nor were Merkel cells present at epiglottal taste buds or the keratin-20-negative fungiform taste buds or elsewhere in rat tongue. Hence, Merkel cells make no contribution to rat fungiform, epiglottal, nasopalatine, or palatal taste buds. Human and rat keratin-20-positive tissues are reported to be endodermal derivatives with the exception of Merkel cells and luminal urothelial cells. In rats the distribution of keratin-20-positive taste buds was in full agreement with the classical view that the posterior third of the tongue is derived from endoderm (keratin-20-positive taste buds), whereas the anterior two-thirds of the tongue is derived from stomadeal ectoderm (keratin-20-negative taste buds). The equally intense keratin 20 immunoreactivity of human fungiform and vallate taste buds violates this traditional rostro-caudal segregation and suggests that endodermally derived tissues may be present in the tip of the human tongue.

Adult↗
PubMed2003

Expression of BDNF and TrkB in mouse taste buds after denervation and in circumvallate papillae during development.

BDNF (brain-derived neurotrophic factor) is a member of the neurotrophin family which affects the proliferation and survival of neurons. Using an immunocytochemical method, we examined the expression of BDNF and its receptor, TrkB, in the taste bud cells of the circumvallate papillae of normal mice and of mice after transection of the glossopharyngeal nerves. We additionally observed the expression of BDNF and TrkB in the developing circumvallate papillae of late prenatal and early postnatal mice. In normal untreated mice, BDNF was expressed in most of the taste bud cells; TrkB was detected in the plasma membrane of taste bud cells and in the nerve fibers. Double-labeling studies showed that BDNF and NCAM (neural cell adhesion molecule) or TrkB and NCAM colocalized in some of the taste bud cells, but that most taste bud cells were immunopositive for only BDNF or TrkB. NCAM-immunoreactive cells are known to be type-III cells, which have afferent synaptic contacts with the nerve terminals. Five days after denervation, the number of taste buds and nerve fibers markedly decreased; however, the remaining taste bud cells still expressed BDNF and TrkB. By 10 days after denervation, most of the taste buds had disappeared, and there were a few TrkB-immunoreactive nerve fibers in the connective tissue core. By 4 weeks after denervation, numerous TrkB-immunoreactive nerve fibers had invaded the papillae, and a few taste buds expressing BDNF and TrkB had regenerated. At E (embryonic day) 15 during development, the circumvallate papillae appeared, and then TrkB-immunoreactive nerve fibers entered the connective tissue core, and some of these fibers further invaded among the dorsal epithelial cells of the papillae. TrkB-immunoreactive oval-shaped cells were occasionally found in the dorsal epithelium. Such TrkB-immunoreactive nerve fibers and cells were also observed at E16-18. However, BDNF was not expressed in the papillae through the late prenatal days of E15 to E18. At P (postnatal day) 0, a cluster of BDNF-and TrkB-immunoreactive cells appeared in the dorsal epithelium of the papillae, and was presumed to be primitive taste buds. We conclude that TrkB-immunoreactive nerve fibers are necessary for papillary and taste bud formation during development and for the regeneration of taste buds after denervation. BDNF in the taste bud cells may act as a neurotrophic factor for innervating sensory neurons--through TrkB receptors of the axons of those neurons, and also may exert autocrine and paracrine trophic actions on neighboring taste bud cells by binding to their TrkB receptors.

Animals↗
PubMed1999

Distribution of vimentin in the developing chick taste bud during the perihatching period.

The tissue environment within which taste bud cells develop has not been wholly elaborated. Previous studies of taste bud development in vertebrates, including the avian chick, have suggested that taste bud cells could arise from one, or several tissue sources (e.g. crest-mesenchyme, local ectoderm or endoderm). Thus, molecular markers which are present in gemmal as well as interfacing (peribud epithelium; mesenchyme-epithelium) regions, and their degree of expression during stages of taste bud development, are of special interest. The intermediate filament protein, vimentin, occurs in mesenchymal and mesodermally-derived (e.g. endothelial, fibroblast) cells as well as highly proliferating epithelium (e.g. tumors). The present study in chick gustatory tissue utilized antibodies against vimentin and the avidin-biotin-peroxidase technique to evaluate vimentin immunoreactivity (IR) within a timeframe which includes: 1) early stages of the taste bud primordium [embryonic days (E)17-E18)]; 2) the beginning of an accelerated bud cell proliferation at the time of initial, taste bud pore opening [around E19]; 3) attaining the adult complement of taste buds [around posthatch (H) day 1], and 4) completed organogenesis (H 17). During this time span, vimentin-IR was characterized in a region including and sometimes bridging taste bud and subepithelial connective tissue, whereas non-gustatory surrounding epithelium and salivary glands were vimentin-immuno-negative. Intragemmally, the proportion of vimentin-IR cells as related to total taste bud cells peaked at E19. These results indicate that vimentin expression, in part, is related to the onset of taste bud cell proliferation and suggest that mesenchyme could be one source of taste bud cells. Secondly, fibronectin, an extracellular matrix component of the epithelial basement membrane interface with mesenchyme, was expressed at or near the apical surfaces of taste bud cells projecting into the bud lumen, and in the basal gemmal region suggesting the possible role of fibronectin as a chemotactic anchor for differentiating and migrating taste bud receptor cells. Lastly, neuron-specific enolase-IR indicates that axonal varicosities are already present intragemmally at E17-E18, that is, during the incipient period of identifiable taste bud primordia.

Animals↗
PubMed2000

Glutamate-induced cobalt uptake reveals non-NMDA receptors in rat taste cells.

Taste receptor cells are chemical detectors in the oral cavity. Taste cells form synapses with primary afferent neurons that convey the gustatory information to the central nervous system. Taste cells may also synapse with other taste cells within the taste buds. Furthermore, taste cells may receive efferent connections. However, the neurotransmitters at these synapses have not been identified. Glutamate, a major excitatory neurotransmitter in other sensory organs, might act at synapses in taste buds. We used a cobalt staining technique to detect Ca(2+)-permeable glutamate receptors in taste buds and thus establish whether there might be glutamatergic synapses in gustatory end organs. When 500 microm slices of foliate and vallate papillae were briefly exposed to 1 mM glutamate in the presence of CoCl(2), a subset of spindle-shaped taste cells accumulated Co(2+). Cobalt uptake showed concentration-dependency in the range from 10 microm to 1 mM glutamate. Interestingly, higher glutamate concentrations depressed cobalt uptake. This concentration-response relation for cobalt uptake suggests that synaptic glutamate receptors, not receptors for glutamate taste, were activated. Sensory axons and adjacent non-sensory epithelium were not affected by these procedures. Glutamate-stimulated cobalt uptake in taste cells was antagonized by the non-NMDA receptor antagonist CNQX. Depolarization with 50 mM K(+) and application of NMDA (300 microM) did not increase the number of stained taste cells. This pharmacological characterization of the cobalt uptake suggests that non-NMDA receptors are present in taste cells. These receptors might be autoreceptors at afferent synapses, postsynaptic receptors of a putative efferent system, or postsynaptic receptors at synapses with other taste cells.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2001

Effects of zinc deficiency on the vallate papillae and taste buds in rats.

BACKGROUND AND PURPOSE: Zinc deficiency is associated with multiple clinical complications, including taste disturbance, anorexia, growth retardation, skin changes, and hypogonadism. We investigated the zinc-deficiency-induced morphologic changes in the vallate taste buds of weanling and young adult male Wistar rats. METHODS: A total of 24 weanling and 30 young adult rats were used. Each age group was further divided into a control group fed a zinc-adequate (50 ppm) diet, a zinc-deficient (< 1 ppm) diet group, and a zinc-adequate pair-fed group who were fed the same amount of food as that taken by the zinc-deficient group. Weanling rats were fed for 4 weeks and young adult rats were fed for 6 weeks. The morphometry and morphologic changes of vallate taste buds were analyzed using light and transmission electron microscopy. RESULTS: Light microscopy revealed no significant difference in papilla size and morphology among the various groups. In both weanling and young adult rats in the zinc-deficient diet and pair-fed groups, the number of taste buds per papilla (per animal) and the average profile area of the taste bud were significantly smaller than those of the corresponding controls (p < 0.05). Ultrastructural changes were seen only in the taste buds of weanling rats fed the zinc-deficient diet, with derangement of the architecture of the taste bud and widening of the intercellular space between taste bud cells. The proportion of type I taste bud cells in the taste buds of weanling rats fed the zinc-deficient diet decreased from 59% to 39%, and that of type II taste bud cells decreased from 25% to 12%. No obvious changes in the ultrastructure of type III taste bud cells were observed. CONCLUSIONS: The main effects of zinc deficiency in weanling and young adult rats and in adequate diet pair-fed rats were changes in the number and size of taste buds, and fine structure changes in the taste bud cells, especially during the accelerated growth stage after weaning.

Aging↗
PubMed1999

Differential calming responses to sucrose taste in crying infants with and without colic.

BACKGROUND: Colic is a behavioral syndrome of early infancy of unknown etiology whose core symptom is increased crying. Both clinical anecdotal descriptions and controlled observations converge in suggesting that a defining characteristic of the crying behavior is the longer duration of the crying bouts, especially during the second month of life when colic is at its peak. This implies that, once infants with colic begin crying, they do not calm as well as infants without colic. To investigate this difference objectively, we used response to sucrose taste as a probe of colic-normal differences in regulation of crying for three reasons. First, sucrose taste has been shown to be a potent regulator of crying in human newborns. Second, convergent evidence from studies in both nonhuman and human infants suggests that sucrose calming reflects the function of central distress regulatory systems that are opioid-dependent. Third, effectiveness of sucrose calming diminishes in normal infants by 4 to 6 weeks of age, consistent with the developmental increase in crying duration common to infants with and without colic. Consequently we predicted that, if the regulation of crying by sucrose taste is relevant to the crying of infants with colic, calming responses to sucrose taste should be less effective in 6-week-old infants with colic compared with those without. OBJECTIVES: To investigate the clinical observation that infants with and without colic differ in their ability to regulate their crying behavior, our primary objective was to determine if there were differential crying responses to intraoral sucrose tastes (relative to water) in crying infants with and without colic. Based on previous studies of calming responses to sucrose taste, it was predicted that sucrose-specific calming before a feeding would be less effective in infants with colic than in those without. A secondary and more exploratory aim was to assess calming responses to sucrose (relative to water) on spontaneous crying after a feed in both groups. METHODS: Nineteen infants meeting modified Wessel's criteria for colic were compared with 19 age- and sex-matched normal infants without colic in a within-subject controlled observation of calming and mouthing responses to both intraoral sucrose and water tastes. Both before and after two feedings on the same day, each infant was observed until she or he cried continuously for 15 consecutive seconds, at which time three 250-microL tastes of 48% sucrose solution or sterile water were administered 30 seconds apart, and infant responses videotaped. Outcome measures derived from second-by-second coding of the videorecordings were percent time crying per minute for 4 minutes and percent time mouthing per minute for 2 minutes after stimulus administration. RESULTS: As predicted, the crying of infants with colic was less affected than the crying of infants without colic after sucrose but not water tastes before feedings. After feedings, the crying of infants with colic was less affected than the crying of infants without colic for both sucrose and water tastes, and sucrose was more effective than water in both groups of infants. These calming differences could not be attributed to differences in mouthing responses because the calming effects persisted after mouthing ceased, and there were no differences in mouthing responses between groups before or after feedings. CONCLUSIONS: As in newborns, a significant calming effect of sucrose taste that persisted beyond the cessation of mouthing could be elicited in crying 6-week-old infants, but it required a stronger taste stimulus to do so. As predicted, infants with colic were less effectively calmed by sucrose taste than infants without. These differential effects could not be accounted for by differences in crying when the stimulus was applied or by differences in mouthing behavior. Before a feed, these differences in calming were specific to sucrose taste. After a feed, infants with c

Colic↗
PubMed2006

Taste perception and coding in the periphery.

Recent identification of taste receptors and their downstream signaling molecules, expressed in taste receptor cells, led to the understanding of taste coding in the periphery. Ion channels appear to mediate detection of salty and sour taste. The sensations of sweet, umami and bitter taste are initiated by the interaction of sapid molecules with the G-protein-coupled receptors T1Rs and T2Rs. Mice lacking either PLCbeta2 or TRPM5 diminish behavioral and nerve responses to sweet, umami and bitter taste stimuli, suggesting that both receptor families converge on a common signaling pathway in the taste receptor cells. Nevertheless, separate populations of taste cells appear to be uniquely tuned to sweet, umami and bitter taste. Since PLCbeta2-deficient mice still respond to sour and salty stimuli, sour and salty taste are perceived independent of bitter, umami and sweet taste. In this review, the recent characterization of the cellular mechanisms underlying taste reception and perception, and of taste coding in the periphery will be discussed.

Action Potentials↗
PubMed1995

Taste and smell losses in HIV infected patients.

Human immunodeficiency virus (HIV-1) associated wasting is an increasingly common clinical manifestation of AIDS. The pathogenesis of wasting is multifactorial and includes reduced caloric intake as a major contributing mechanism. The perceptions of taste and smell play an important role in stimulating caloric intake and in optimizing nutrient absorption through cephalic phase reflexes. The purpose of this study was to evaluate the degree of losses in taste and smell function that occur in subjects infected with HIV. Taste and smell function was evaluated in 40 HIV infected individuals and 40 healthy control subjects matched for age, sex, race, smoking behavior, and number of years of education. Chemosensory tests administered to subjects included taste and smell detection thresholds, taste and smell memory tests, taste and smell discrimination tests, and taste and smell identification tasks. Significant differences were observed between experimental and control subjects in glutamic acid taste detection threshold (p < 0.001), quinine hydrochloride taste detection threshold (p < 0.001), menthol smell detection threshold (p < 0.001) and in the taste identification task (p = 0.006). Overall the results suggest abnormalities in the peripheral and central nervous systems, and subjective distortion of taste and smell. A significant correlation was not established between CDC classification of HIV infection and taste and smell function, although trends were observed suggesting worsening function with progression of HIV disease. These results document significant taste and smell losses in HIV infected subjects which may be of clinical significance in the development or progression of HIV associated wasting.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Electrophysiology of Necturus taste cells.

Taste buds are sensory end organs that detect chemical substances occurring in foodstuffs and relay the relative information to the brain. The mechanisms by which the chemical stimuli are converted into biological signals represent a central issue in taste research. Our understanding of how taste buds accomplish this operation relies on the detailed knowledge of the biological properties of taste bud cells-the taste cells-and of the functional processes occurring in these cells during chemostimulation. The amphibian Necturus maculosus (mudpuppy) has proven to be a very useful model for studying basic cellular processes of vertebrate taste reception, some of which are still awaiting to be explored in mammals. The main advantages offered by Necturus are the large size of its taste cells and the relative accessibility of its taste buds, which can therefore be handled easily for experimental manipulations. In this review, I summarize the functional properties of Necturus taste cells studied with electrophysiological techniques (intracellular recordings and patch-clamp recordings). My focus is on ion channels in taste cells and on their role in signal transduction, as well as on the functional relationships among the cells inside Necturus taste buds. This information has revealed to be well suited to outline some of the general physiological processes occurring during taste reception in vertebrates, including mammals, and may represent a useful framework for understanding how taste buds work.

Action Potentials↗
PubMed1995

Selective inhibition of bitter taste of various drugs by lipoprotein.

Previously, we demonstrated that lipoprotein composed of phosphatidic acid (PA) and beta-lactoglobulin (LG) selectively and reversibly suppress the frog taste nerve response to bitter substances. In the present study, we examined the effects of various lipoproteins on the taste sensation to various stimuli in humans by a psychophysical method. Among various lipoproteins composed of different of lipids and proteins, the lipoproteins composed of PA and proteins were most effective in suppressing bitter taste. The lipoproteins composed of PA and LG, bovine serum albumin, ovalbumin, alpha-lactoalbumin or casein similarly suppressed effects on sensation of bitter taste. Using PA-LG, the effects on taste sensation to various stimuli were examined. The bitter taste of all twelve substances examined was inhibited, while saltiness of NaCl and sweetness of sucrose were not inhibited. The inhibition of bitter taste was completely reversible. Masking of the target sites for bitter substances on the taste receptor membranes with PA-LG seems to contribute to the inhibition of bitter taste. Direct binding of the bitter substances to PA-LG in the medium also contributes to the inhibition of bitter taste of certain substances. Among various drugs, basic and hydrophobic substances such as quinine, denatortium and propranolol have low taste thresholds and are said to be the most bitter. PA-LG most effectively suppressed the bitter taste of such substances. PA originates from soybeans and the proteins used except for bovine serum albumin originate from milk or eggs, and hence the lipoproteins can be safely used to mask the bitter taste of drugs.

Caffeine↗
PubMed2001

Age-related alteration of taste bud distribution in the common marmoset.

Alteration in the number of taste buds on the soft palate (SP), fungiform (FF), foliate (FL) and circumvallate (CV) papillae in the common marmoset at different postnatal ages was examined histologically. After paraffin embedding, complete serial sections at 10 microm thickness were made and stained by HE. Digitized images for each section were examined carefully. The number of FF taste buds at day 1 was 334. While only 20% of all the taste buds at birth possessed a taste pore, 39% of 174 SP taste buds at day 1 possessed a taste pore. The number of taste buds with pores at day 1 was small for the center CV (19 of 59), one side CV (7 of 25), and one side FL (2 of 16). These results suggest that the functional maturation of SP taste buds may precede maturation in other areas of the tongue. The total number of taste buds increased with increasing age, reached a maximum at 2 months of age: FF, 1069; SP, 609; CV-center, 530; CV-side, 390; FL, 201, and decreased thereafter. Almost all taste buds possessed a taste pore after 2 months of age. The decrease in the number of taste buds in the oral cavity with increase in age may change taste sensitivity.

Aging↗
PubMed2000

Heterogeneity of fish taste bud ultrastructure as demonstrated in the holosteans Amia calva and Lepisosteus oculatus.

Taste buds are the peripheral sensory organs of the gustatory system. They occur in all taxa of vertebrates and are pear-shaped intra-epithelial organs of about 80 microm height and 50 microm width. Taste buds mainly consist of specialized epithelial cells, which synapse at their bases and therefore are secondary sensory cells. Taste buds have been described based on studies of teleostean species, but it turned out that the ultrastructure of teleostean taste buds may differ between distinct systematic groups and that this description is not representative of those taste buds in other main taxa of fishes, such as selachians, holosteans and dipnoans. Furthermore, it is not known how variable the micromorphologies of non-teleostean taste buds are. For this reason the taste buds of two holosteans, Lepisosteus oculatus and Amia calva, were investigated and compared. While in both species the taste buds are of the same shapes and sizes, the cellular components of their sensory epithelia differ: in Lepisosteus taste buds comprise two types of elongated light cells and one type of dark cells. In contrast, Amia taste buds contain only one type of light, but two types of dark elongated cells. Afferent synapses are common in the buds of both species, efferent synapses occur only in Lepisosteus taste buds. These differences show that even in the small group of holostean fishes the taste buds are differently organized. Consequently, a representative type of fish taste buds does not exist.

Animals↗
PubMed1997

Responses to glutamate in rat taste cells.

We studied taste transduction in sensory receptor cells. Specifically, we examined the actions of glutamate, a significant taste stimulus, on the membrane properties of taste cells by applying whole cell patch-clamp techniques to cells in rat taste buds isolated from foliate and vallate papillae. In 55 of 91 taste cells, bath-applied glutamate, at concentrations that elicit taste responses in the intact animal (10-20 mM), produced one of two different responses when the cell membrane was held near its presumed resting potential, -85 mV. "Sustained" glutamate responses were observed in the majority of taste cells (51 of 55) and consisted of an outward current (reduction of the maintained inward current). Sustained glutamate responses were voltage dependent, were decreased by membrane depolarization, and were accompanied by a reduction in membrane conductance. An analysis of the reversal potential of sustained responses in different ionic conditions and the effect of ion substitutions suggested that the currents were carried by cations. The data suggest that sustained responses are mediated by the closure of nonselective cation channels. Other taste cells (4 of 55) responded to glutamate with a transient inward current--so-called "transient" responses. Transient glutamate responses were voltage dependent and Na+ dependent, and appeared to be generated by nonspecific cation channels activated by glutamate. L(+)-2-amino-4-phosphonobutyric acid (L-AP4), a specific agonist of a metabotropic glutamate receptor (mGluR4) recently identified in rat taste cells and believed to be involved in taste transduction, mimicked the sustained glutamate responses. These findings indicate that glutamate, at concentrations at or slightly above threshold for taste in rats, produces two different membrane currents. The properties of these two responses suggest that there may be two different sets of nonspecific cation channels in taste cells, one closed by glutamate (sustained response) and the other opened (transient response). Our findings on the effect of L-AP4 suggest that the sustained response is the membrane mechanism mediating, at least in part, taste transduction for glutamate.

Animals↗
PubMed1994

Fine structure of taste buds located on the lamb epiglottis.

BACKGROUND: Taste buds located on the aryepiglottal folds and laryngeal surface of the epiglottis are the principal receptors responsible for the initiation of the laryngeal chemoreflex. In contrast to the wealth of information available concerning the ultrastructure of oral taste buds, little comparable data exists for taste buds located at the entrance to the larynx. Therefore, the present study was designed to investigate the fine structure of taste buds located on the lamb epiglottis. MATERIALS: Stained thick and semi-serial thin sections from taste buds located on the lamb epiglottis were examined with light and electron microscopy. RESULTS: Based on morphological criteria, three types of cells could be identified in the taste bud: Type I, Type II, and basal cells. Both Type I and Type II cells extended into the apical taste pore, but there were differences between these two cell types with regard to nuclear profiles, electron density, and the relative density of ribosomes, apical mitochondria, and rough and smooth endoplasmic reticulum. Basal cells did not extend a process into the taste pore. Nerve processes were observed throughout the taste bud. Synapses were observed between both Type I and Type II cells and nerve fibers. These synapses exhibited membrane thickenings and accumulations of clear and dense-cored vesicles of varying proportions in the taste cell cytoplasm adjacent to membrane specializations. CONCLUSIONS: The taste buds located on the lamb epiglottis share several structural similarities to taste buds located in the oral cavity and other regions of the pharynx and larynx of many mammalian species. The presence of synapses on both Type I and Type II cells of the lamb epiglottal taste bud suggests that both cell types are involved in laryngeal chemoreception.

Animals↗
PubMed1987

Neural induction of taste buds.

Bilateral innervation allows more than 80% of the 610 vallate taste buds to survive removal of one IXth nerve in adult rats. Removal of both IXth nerves in neonatal or adult rats results in the absence of taste buds. In studying development, we found that removing or crushing one IXth nerve in three-day-old neonates profoundly decreased the number of vallate taste buds that subsequently developed. Specifically, after removal of one IXth nerve at 3 days, only 228 taste buds formed, compared with 496 taste buds that one nerve would maintain in adults. Thus, during normal development, the right and left IXth nerves interact synergistically, as at least 150 more taste buds develop than predicted by the sum of the independent action of each IXth nerve. This suggests that vallate taste buds are induced by the IXth nerve. A second example of synergism, representing evidence for the neural induction of taste buds, came from experiments in which we crushed the left IXth nerve 3 days after birth and found that these regenerated IXth nerve axons induced 4 times as many taste buds in the presence of the normal right IXth nerve (118 taste buds) as in its early absence (30 taste buds). We conclude that taste buds are neurally induced and that axons of the IXth nerve interact synergistically in inducing them, rather than competing for targets. We propose that in development innervated progenitor cells form stem cells which lead to taste bud cells.

Animals↗
PubMed1993

Evidence for stimulus access to taste cells and nerves during development: an electron microscopic study.

We have examined developing taste buds in fungiform papillae of rats from the 18th day of gestation (E18) to the 15th postnatal day (P15). Nerve processes were seen in the epithelium of E18 rats before taste buds were obvious. At E20, early taste buds were visible, but were embedded within the epithelium, i.e., their cells were shielded from the oral cavity by overlying squamous epithelium. At this stage, the epithelium on the lateral aspects of the fungiform papillae was keratinized, but that overlying the taste bud was not. Some taste bud cells at E20 contained synapse-like structures near their contacts with nerve processes. In postnatal animals, keratinized epithelial cells were seen overlying taste buds, but taste pores were not observed until P10. How, then, do stimuli reach the taste cells and elicit physiological and behavioral responses as reported by others? The keratinized epithelium overlying the buds was unlike that on the lateral aspect of the papilla in at least one significant way. Few lamellated bodies were present in intercellular spaces beneath the stratum corneum, whereas these were abundant in the corresponding location within epithelium on the slope of the papilla. Although some were present within the squamous epithelium overlying the bud, they apparently were not released into the intercellular space. These lipid-rich lamellated bodies are thought to represent the water barrier of the epithelium, i.e., the barrier which prevents aqueous solutions from passing through the epithelium. We determined that the keratinized epithelium overlying the taste bud was permeable to a tracer, lanthanum nitrate, whereas that on the lateral surface was not. Lanthanum was visualized around taste cells and around nerve profiles within and near the taste bud. We propose that the absence of an aqueous permeability barrier in the epithelium overlying taste buds likely explains the ability of tastants to reach the taste bud cells and nerves in the developmental period before pore formation.

Animals↗
PubMed2004

Taste aversion learning induced by forced swimming in rats.

Two experiments demonstrated that forced swimming endowed rats with aversion to the taste solution consumed before the swimming. In Experiment 1, the rats given a trial of taste-swimming sequence drank less of the taste solution in a later test than did the rats given a taste-alone trial. The rats given a trial of taste-poisoning-swimming sequence, however, drank more of the taste solution in the testing than did the rats given a trial of taste-poisoning sequence. These results suggest that some effects of swimming (e.g., energy expenditure caused by physical exercise) induce conditioned taste aversion although they attenuate taste aversion conditioned by poisoning. The attenuation of poison-induced taste aversion by swimming has been reported in the literature, but the swimming-induced taste aversion is novel. Experiment 2, accordingly, was planned to confirm this phenomenon with a differential conditioning procedure, where one of two taste solutions was paired with swimming while the other was not. After a few repetitions of these two types of trials, the rats' intakes of these two solutions were differentiated to show that swimming has the ability to cause taste aversion.

Animals↗