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Contribution of alpha-gustducin to taste-guided licking responses of mice.

We examined the necessity of alpha-gustducin, a G protein alpha-subunit expressed in taste cells, to taste-mediated licking responses of mice to sapid stimuli. To this end, we measured licking responses of alpha-gustducin knock-out (Gus-/-) mice and heterozygotic littermate controls (Gus+/-) to a variety of 'bitter', 'umami', 'sweet', 'salty' and 'sour' taste stimuli. All previous studies of how Gus-/- mice ingest taste stimuli have used long-term (i.e. 48 h) preference tests, which may be confounded by post-ingestive and/or experiential effects of the taste stimuli. We minimized these confounds by using a brief-access taste test, which quantifies immediate lick responses to extremely small volumes of sapid solutions. We found that deleting alpha-gustducin (i) dramatically reduced the aversiveness of a diverse range of 'bitter' taste stimuli; (ii) moderately decreased appetitive licking to low and intermediate concentrations of an 'umami' taste stimulus (monosodium glutamate in the presence of 100 microM amiloride), but virtually eliminated the normal aversion to high concentrations of the same taste stimulus; (iii) slightly decreased appetitive licking to 'sweet' taste stimuli; and (iv) modestly reduced the aversiveness of high, but not low or intermediate, concentrations of NaCl. There was no significant effect of deleting alpha-gustducin on licking responses to NH4Cl or HCl.

Animals↗

Expression of T1Rs and gustducin in palatal taste buds of mice.

The palatal region of the oral cavity in rodents houses 100-300 taste buds and is particularly sensitive to sweet and umami compounds; yet, few studies have examined the expression patterns of transduction-related molecules in this taste field. We investigated the interrelationships between members of the T1R family and between each T1R and gustducin in palatal taste buds. Similar to lingual taste buds, T1R1 and T1R2 are generally expressed in separate palatal taste cells. In contrast to lingual taste buds, however, T1R2 and T1R3-positive palatal taste cells almost always coexpress gustducin, suggesting that sweet taste transduction in the palate is almost entirely dependent on gustducin. T1R1-positive palate taste cells coexpress gustducin about half the time, suggesting that other G proteins may contribute to the transduction of umami stimuli in this taste field.

Animals↗

Influences of aging on taste perception and oral somatic sensation.

BACKGROUND: Many elderly persons report reduced taste perception of the foods they eat. Any disturbance of taste and oral somatic sensations can induce this phenomenon. To determine the cause of decreased taste perception in older persons, the authors investigated age-related changes in taste perception and somatic sensations in the anterior tongue. METHODS: Thirty healthy young and elderly persons participated in this study. Recognition thresholds of four basic tastes (sweet, salty, sour, and bitter) and the threshold of irritating sensation induced by capsaicin were measured by local stimulation using filter-paper disks. Two-point discrimination thresholds were measured to evaluate the spatial acuity of touch sensation. All measurements were carried out at the tip of the dorsal tongue. RESULTS: The recognition thresholds of all four basic tastes of elderly participants were significantly higher than those of young participants. On the contrary, age-associated changes were not observed in 2-point discrimination and capsaicin sensation. CONCLUSIONS: Significant age-associated deterioration was observed in taste but not somatic sensations such as touch and burning pain in the tongue, showing that aging affects taste perception and oral somatic sensations differently. This suggests that decreased taste perception of foods in elderly people may be caused primarily by perceptual loss of taste among oral sensations.

Adolescent↗

Taste reception.

Recent research on cellular mechanisms of peripheral taste has defined transduction pathways involving membrane receptors, G proteins, second messengers, and ion channels. Receptors for organic tastants received much attention, because they provide the specificity of a response. Their future cloning will constitute a major advance. Taste transduction typically utilizes two or more pathways in parallel. For instance, sweet-sensitive taste cells of the rat appear to respond to sucrose with activation of adenylyl cyclase, followed by adenosine 3',5'-cyclic monophosphate (cAMP)-dependent membrane events and Ca2+ uptake. The same cells respond differently to some artificial sweeteners, i.e., with activation of phospholipase C (PLC) followed by inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release from intracellular stores. Some bitter tastants block K+ channels or initiate the cascade receptor G1 protein, PLC, IP3, and Ca2+ release or the cascade receptor alpha-gustducin, phosphodiesterase (PDE), cAMP decrease, and opening of cAMP-blocked channels. Membrane-permeant bitter tastants may elicit a cellular response by interacting with G protein, PLC, or PDE of the above cascades. Salt taste is initiated by current flowing into the taste cell through cation channels located in the apical membrane, even though basolateral channels may also contribute (following salt diffusion through paracellular pathways). In rodents, the Na+-specific component of salt taste is typically mediated by apical amiloride-sensitive Na+ channels, but less specific and not amiloride-sensitive taste components exist in addition. Sour taste may in part be mediated by amiloride-sensitive Na+ channels conducting protons, but other mechanisms certainly contribute. Thus the transduction of taste cells generally comprises parallel pathways. Furthermore, the transduction pathways vary with the location of taste buds on the tongue and, of course, across species of animals. To identify these pathways, to understand how they are controlled and why they evolved to this complexity are major goals of present research.

Animals↗

Taste impairment and related factors in type I diabetes mellitus.

To study taste in type I (insulin-dependent) diabetes mellitus, 57 consecutive diabetic outpatients (mean +/- SE duration of diabetes 11.4 +/- 0.4 yr) and 38 control subjects were screened for taste disorders with electrogustometry and chemical gustometry. Both groups were comparable for all subject characteristics except body mass index, which was higher in the diabetic group (P less than .05). A taste impairment was found in the diabetic group relative to the control group with electrogustometry (mean threshold 184.3 +/- 15.8 vs. 58.7 +/- 9.2 microA; P less than .001) and chemical gustometry (mean score 13.2 +/- 0.7 vs. 17.1 +/- 0.8; P less than .001). Hypogeusia was found among 73% of the diabetic patients versus 16% of the control subjects (P less than .001). The four primary tastes were involved in taste impairment. With multivariate analysis, taste disorders were related to diabetic status and tobacco and alcohol consumption. In the diabetic group, taste impairment was significantly associated with complications and duration of disease. With multivariate analysis, peripheral neuropathy had the strongest association with taste disorders. These results suggest that taste is impaired during the course of type I diabetes mellitus and that taste impairment could be a complication of the disease. A mechanism of the neuropathic type could be involved.

Adult↗

Expression of sonic hedgehog, patched, and Gli1 in developing taste papillae of the mouse.

Lingual taste buds form within taste papillae, which are specialized structures that develop in a characteristic spatial and temporal pattern. To investigate the signaling events responsible for patterning and morphogenesis of taste papillae, the authors examined the time course and distribution of expression of several related developmental signaling genes as well as the time course of innervation of taste papillae in mouse embryos from embryonic day 12 (E12) to E18. Lingual expression of the signaling molecule Sonic hedgehog (Shh), its receptor Patched (Ptc), and the Shh-activated transcription factor Gli1 were assayed by using in situ hybridization. Shh is expressed broadly in the lingual epithelium at E12 but becomes progressively restricted to developing circumvallate and fungiform papillary epithelia. Shh is expressed specifically within the central cells of the papillary epithelium starting at E13.5 and persisting through E18. Ptc and Gli1 expression follow a pattern similar to that of Shh. Compared with Shh, Ptc is expressed in larger regions surrounding the central papillary cells and also in the mesenchyme underlying Shh-expressing epithelium. Innervation of taste papillae was examined by using the panneuronal antibody to ubiquitin carboxyl terminal hydrolase (protein gene product 9.5). Nerves reach the basal lamina of developing taste papillae at E14 to densely innervate the papillary epithelium by E16. Thus, the pattern of Shh expression within developing taste papillae is established prior to innervation, ruling out neuronal induction of papillae. The results suggest that the Shh signaling pathway may be involved in: 1) establishing papillary boundaries in taste papilla morphogenesis, 2) papillary epithelial-mesenchymal interactions, and/or 3) specifying the location or development of taste buds within taste papillae.

Animals↗

Cellular expression of alpha-gustducin and the A blood group antigen in rat fungiform taste buds cross-reinnervated by the IXth nerve.

Although taste buds are trophically dependent on their innervation, cross-reinnervation experiments have shown that their gustatory sensitivities are determined by the local epithelium. Both the gustatory G-protein, alpha-gustducin, and the cell-surface carbohydrate, the A blood group antigen, are expressed by significantly fewer fungiform than vallate taste cells in the rat. In these experiments, one side of the anterior portion of the tongue was cross-reinnervated by the IXth nerve in order to determine whether the molecular expression of taste bud cells is determined by the epithelium from which they arise or by the nerve on which they are trophically dependent. The proximal portion of the IXth nerve was anastomosed to the distal portion of the chorda tympani (CT) nerve using fibrin glue (IX-CT rats). Control animals had the CT cut and reanastomosed using the same technique (CT-CT rats), or had the CT avulsed from the bulla and resected to prevent regeneration (CTX rats). The animals survived for 12 weeks postoperatively, and the tongues were removed, stained with methylene blue, and the fungiform taste pores counted on both sides. Tissue from the anterior 5 mm of the tongue was cut into 50-microm sections, which were incubated with antibodies against alpha-gustducin and the human blood group A antigen. In both CT-CT and IX-CT rats, there was regeneration of fungiform taste buds, although in both groups there were significantly fewer taste buds on the operated side of the tongue. The normal vallate papilla had a mean of 8.37 alpha-gustducin-expressing cells and 5.22 A-expressing cells per taste bud, whereas the fungiform papillae contained 3.06 and 0.23 cells per taste bud, respectively. In both CT-CT and IX-CT rats there was a normal number of cells expressing alpha-gustducin or the A antigen in regenerated taste buds; in the CTX animals there was a significant decrease in the expression of these markers. These results demonstrate that the molecular phenotype of taste bud cells is determined by the local epithelium from which they arise and not by properties of the innervating nerve.

ABO Blood-Group System↗

A randomized, controlled clinical trial to evaluate the effects of zinc sulfate on cancer patients with taste alterations caused by head and neck irradiation.

BACKGROUND: In uncontrolled clinical trials, the administration of oral zinc sulfate has been reported both to prevent and correct taste abnormalities in cancer patients receiving external radiotherapy (ERT) to the head and neck region. METHODS: Eighteen patients were randomized to receive either zinc sulfate tablets (a dose of 45 mg) or placebo tablets three times a day at the onset of subjective perception of taste alterations during the course of ERT and up to 1 month after ERT termination. Taste acuity was determined by measuring detection and recognition thresholds for four taste qualities. Intolerance of zinc sulfate or placebo administration was investigated, and the oral cavity was examined. All the evaluations were studied prior to, at weekly intervals during, and 1 month after ERT administration. RESULTS: Taste acuity for one or more taste qualities was already impaired before ERT. During ERT treatment, taste alterations were experienced at least once for a minimum of 3 of the 8 measured thresholds by 100% of the patients, and 33.3% of the patients became aware of some alteration within the first week of treatment. The patients treated with placebo experienced a greater worsening of taste acuity during ERT treatment compared with those treated with zinc sulfate. One month after ERT was terminated, the patients receiving zinc sulfate had a quicker recovery of taste acuity than those receiving placebo. Statistically significant differences between the two groups emerged for urea detection and sodium chloride recognition thresholds during ERT treatment and for sodium chloride, saccharose, and hydrogen chloride recognition thresholds after the termination of ERT treatment. CONCLUSIONS: This pharmacologic therapy is effective and well tolerated; it could become a routine in clinical practice to improve the supportive care of patients with taste alterations resulting from head and neck cancer.

Administration, Oral↗

Synaptic proteins in rat taste bud cells: appearance in the Golgi apparatus and relationship to alpha-gustducin and the Lewis(b) and A antigens.

Taste receptor cells are continuously replaced during the life of the animal, but many of their sensory axons respond primarily to stimuli belonging to a single taste quality. This suggests that a newly arising taste cell must form a synapse with an appropriate sensory axon, requiring cell recognition that is likely to be mediated by surface markers. As an approach to studying this process, we attempted to locate synapses by immunolabeling taste buds of rats for proteins involved in neurotransmitter release. In taste bud cells of vallate papillae and nasoincisor ducts, double-labeling experiments showed that syntaxin-1, SNAP-25, synaptobrevin, and synaptophysin colocalized with the Golgi marker beta COP in elongated cytoplasmic compartments that extended from the perinuclear region into apical and basal processes of the cells. Labeled cells were spindle-shaped, identifying them as light cells. Syntaxin-1 appeared only in taste cells, but SNAP-25, synaptobrevin, and synaptophysin were also seen in nerve fibers. The synaptic vesicle glycoprotein SV2 appeared only in nerve fibers. Taste cells of fungiform papillae did not show immunoreactivity for presynaptic proteins or Golgi markers, but axonal labeling was similar to that in other regions. Taste cells with alpha-gustducin could express either presynaptic proteins or the carbohydrate blood group antigen Lewis(b), but not both. Therefore, Lewis(b) and presynaptic proteins are not expressed during the same period in the life of a taste bud cell. Most taste cells expressing syntaxin-1 (82%) also expressed the A blood group antigen, whether or not they expressed alpha-gustducin.

Animals↗

Brain-derived neurotrophic factor is present in adult mouse taste cells with synapses.

Brain-derived neurotrophic factor (BDNF), one of the members of the nerve growth factor family of neurotrophins, is expressed in developing gustatory papillae and is thought to be the neurotrophin that supports gustatory innervation during development. BDNF expression does not cease after development but continues in some taste cells of adult mice. To determine which types of taste cells produce BDNF, we undertook an immunohistochemical study of taste cells in BDNF(LacZ) gene targeted "knock-in" adult mice. In these mice, beta-galactosidase (beta-gal) immunoreactivity is an indicator of cells that produce BDNF transcripts. In the tongues of adult BDNF(LacZ) mice, beta-gal (BDNF) is present in long slender taste cells, as well as pyriform taste cells. Bromodeoxyuridine labeling experiments in BDNF(LacZ) mice indicate that BDNF is not present in taste cells that are younger than 3 days postmitotic. BDNF mainly colocalizes with markers of type II and type III taste cells: ubiquitin carboxyl terminal hydrolase (PGP 9.5), serotonin (5-HT), neural cell adhesion molecule (N-CAM), synaptic associated protein of 25 kDa (SNAP-25), and to a lesser extent with alpha-gustducin. beta-Gal immunoreactivity is not associated with blood group H antigen, a marker of type I taste cells. We conclude that BDNF is absent from basal cells and type I (blood group H antigen immunoreactive) taste cells but is present in differentiated type II and type III taste cells. The presence of SNAP-25 in BDNF-expressing cells suggests a role for BDNF in synaptic formation and transmission.

Animals↗

"Type III" cells of rat taste buds: immunohistochemical and ultrastructural studies of neuron-specific enolase, protein gene product 9.5, and serotonin.

Taste buds contain a variety of morphological and histochemical types of elongate cells. Serotonin, neuron-specific enolase (NSE), ubiquitin carboxyl terminal hydrolase (PGP 9.5), and neural cell adhesion molecule (N-CAM) all have been described as being present in the morphologically defined Type III taste cells in rats. In order to determine whether these substances coexist in a single cell, we undertook immunohistochemical and ultrastructural analysis of taste buds in rats. Double-label studies show that PGP 9.5 and NSE always colocalize. In contrast, PGP 9.5 and serotonin seldom colocalize. Further, whereas the serotonin-immunoreactive cells are always slender and elongate, the PGP 9.5/NSE population comprise two morphological types--one slender, the other broader and pyriform. Although gustducin-immunoreactive taste cells appear similar in overall shape to the pyriform PGP 9.5/NSE population, gustducin never colocalizes with PGP 9.5 or NSE. The serotonin-immunoreactive taste cells have an invaginated nucleus, synaptic contacts with nerve fibers, and taper apically to a single, large microvillus. These are all characteristics of Type III taste cells described previously in rabbits (Murray [1973] Ultrastructure of Sensory Organs I. Amsterdam: North Holland. p 1-81). PGP 9.5-immunoreactive taste cells exhibit two morphological varieties. One type is similar to the serotonin-immunoreactive population, containing an invaginated nucleus, synapses with nerve fibers, and a single large microvillus. The other type of PGP 9.5-immunoreactive taste cell has a large round nucleus and the apical end of the cell tapers to a tuft of short microvilli, which are characteristics of Type II taste cells. Thus, in rats, some Type III cells accumulate serotonin but do not express PGP 9.5, whereas others express PGP 9.5 but do not accumulate amines. Similarly, Type II taste cells come in at least two varieties: those immunoreactive for gustducin and those immunoreactive for PGP 9.5.

Animals↗

Immunolocalization of different forms of neural cell adhesion molecule (NCAM) in rat taste buds.

Taste buds consist of approximately 100 taste cells, including three morphological types of short receptor cells which synapse on the peripheral gustatory nerves. Some of the receptor cells produce neural cell adhesion molecule (NCAM), which may play a role in formation of specific connections in this system. Antibodies directed against different forms of NCAM were utilized in an attempt to define not only the distribution, but also the type of NCAM within taste buds. Within each taste bud approximately 10% of the taste cells exhibit abundant immunoreactivity for 180 kD (ld) or 140 kD (sd) forms of NCAM (i.e., those with an intracellular domain) along virtually the entire surface of the cell. Ultrastructural analysis reveals that these abundantly immunoreactive taste cells are of the intermediate morphological type, although not all of the intermediate taste cells within any bud are immunoreactive. In addition, the ultrastructural studies show that punctate (ld/sd) NCAM-immunoreactivity occurs on the membranes of taste cells and nerve fibers throughout each taste bud. The embryonic form of NCAM (E-NCAM), rich in polysialic acid residues, is present only in association with nerve fibers and other unidentified elongate, thin profiles of a few taste buds. The nerve plexus beneath the gustatory epithelium is also rich in NCAM-immunoreactivity. These fibers occasionally reveal immunoreactivity indicative of only the 120 kD (ssd) form of NCAM, typical of glial cells.

Animals↗

Taste bud expression of human blood group antigens.

Some human blood group antigens are expressed by rodent epithelial cells at different stages of differentiation. Since adult taste cells are continually replaced throughout life, we investigated the expression of the H, B, A and Lewisb blood group determinants by cells of the rat fungiform, foliate and vallate papillae. We employed antibodies against the trisaccharide structures of the H, B, and A blood group antigens and against the Lewisb blood group epitope in studies of normal and denervated taste buds. The antibody against the H antigen reacted with the majority of cells in all taste buds and with cells in the spinous layer of the tongue epithelium. The B antigen was expressed by the majority of taste cells but not by other epithelial cells. The expression of the A antigen was significantly less in the fungiform taste buds than in the vallate or foliate taste buds. The A antigen was also abundantly expressed in the acini of the lingual salivary glands. The Lewisb epitope was expressed by a subset of cells in taste buds of the fungiform, foliate and vallate papillae. Taste buds are trophically dependent upon gustatory nerve innervation. Transection of the chorda tympani or the IXth nerve resulted in the loss of expression of these molecules from the gustatory epithelium, indicating that they are expressed only on differentiated taste cells. The blood group antigens are lactoseries carbohydrates; they are differentially expressed in developing cochlear hair cells and olfactory neurons and may play roles in cell-cell recognition, adhesion, and other interactions important in the developing nervous system. They could have similar functions in the taste and olfactory systems, where the receptors are continually renewed and new synapses between the receptors and their neural targets continually form.

ABO Blood-Group System↗

Development of altered taste preferences in tumor-bearing rats.

Experimental tumors induce a decline in food intake that may derive from changes in taste or the development of taste aversions. The preferences of tumor-bearing (TB) and non-tumor-bearing (NTB) rats for five chemicals (three palatable and two aversive taste stimuli) were studied in an animal model of experimental cancer employing the methylcholanthrene (MCA) sarcoma. In protocol 1, five groups of Fischer 344 rats were given 23-h, two-bottle preference tests (taste solution vs. water) daily from day 3 after tumor implantation until spontaneous death occurred. Both NTB and TB rats avoided quinine hydrochloride and hydrochloric acid solutions throughout the experiment indicating that tumor growth produced no disruption in the animals' perception of these normally aversive tastes. In both groups, preference for sucrose (88% to 97%) and saccharin (75% to 93%) remained high until days 22 and 17 respectively, but tended to decline with advanced tumor growth. In both cases, a reduction in total calorie intake preceded the changes in sucrose or saccharin preference by several days. With or without a tumor, rats exhibited approximately 50% preference for NaCl at all times. In protocol 2, a four-bottle preference test (sucrose vs. saccharin vs. NaCl vs. water) was administered before tumor implantation and again 3 weeks later when a decline in food intake was evident. Both TB and NTB rats displayed a dominant preference for sucrose over saccharin, NaCl, and water at the pre- and posttests. However, a comparison of the difference scores (pre- minus postimplantation) of NTB and TB rats showed a small but significant suppression of TB animals' preference for sucrose. The altered preferences for sweet but not salt taste stimuli suggest that food-related taste cues may be more susceptible to the development of taste aversions during cancer. However the contribution of taste changes to the anorexia of cancer remains unclear and it is possible that the changes in taste preference may be secondary to the reduction in food intake.

Animals↗

TUNEL staining and electron microscopy studies of apoptotic changes in the guinea pig vallate taste cells after unilateral glossopharyngeal denervation.

On the basis of our previous report that unilateral glossopharyngeal neurectomy in the guinea pig resulted in degeneration and disappearance of taste buds in ipsilateral vallate papillae (Huang and Lu 1996), it is reasonable to speculate that gustatory denervation may enhance apoptosis of taste bud cells, with taste buds decreasing in number and ultimately disappearing after neurectomy. We were therefore determined to investigate apoptosis of taste bud cells in guinea pig vallate papillae after unilateral glossopharyngeal neurectomy using both terminal deoxynuleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL) at the light microscopic level and by conventional electron microscopy. A total of 34 adult guinea pigs were unilaterally glossopharyngeal-neurectomized and sacrificed at 3, 6, 12 h and 1, 3 and 7 days after surgery. The results revealed that only a very few TUNEL-positive nuclei indicating apoptosis were present in normal taste buds, but in surgically denervated papillae, they increased in number from 6 h-12 h after surgery, reached at peak on day 1 and then gradually decreased. In apoptotic cells from normal taste buds, electron microscopy revealed condensation of the chromatin against the nuclear envelope, changes in the nuclear envelope, and fragmentation of the nucleus, but the integrity of the plasma membrane and organelles was maintained. Neurectomized taste cells were also characterized by condensed and fragmentary nuclei, compactness of the cytoplasmic organelles, and the appearance of pedunculated protuberances on the cell surface. From these observations, we conclude that: (1) glossopharyngeal neurectomy enhanced apoptosis of vallate taste bud cells in guinea pig; (2) appropriate gustatory nerve innervation is an essential component for the maintenance of the taste bud, and may play a role in apoptosis of taste cells.

Animals↗

Quantitative taste bud distribution in the hamster.

The distribution of taste buds was examined in hamsters to reveal the sources of convergent neural activity on taste neurons of the medulla and pons. A total of 723 taste buds was found in adult animals. Fungiform papillae contained 130 taste buds (18%). A single vallate papilla had 168 taste buds (23%). There were 230 taste buds (32%) located on bilateral foliate papillae. The palate contained 100 taste buds (14%) divided among the soft palate (88, 12%) and the incisal papilla (12, 2%). On the epiglottis and adjacent region of the esophagus were found 70 taste buds (10%). About 10 taste buds each were located on the buccal wall (1.4%), while the remaining 5 taste buds were found on the sublingual organ. Conclusions about information processing in central neurons of the gustatory system must reflect knowledge of diverse receptor populations and their interactions.

Animals↗

Conditioned reversal of reactions to normally avoided tastes.

Oral motor responses, elicited by the infusion of a taste solution into a rat's mouth, can be changed through association with either other tastes or internal states. Such changes have been well established when ingestive responses, elicited by a normally preferred taste, are changed to aversive responses when the taste signals a LiCl injection. However, the converse has yet to be clearly established; that aversive responses, elicited by a normally avoided taste, can be changed to ingestive responses in a nondeprived animal, as a result of conditioning. We demonstrate here that when a normally avoided taste (quinine or HCl) signals a preferred taste (sucrose), the oral motor responses gradually undergo two types of change as a function of trials. The aversive oral motor responses elicited by the avoided taste decrease over trials and the ingestive responses increase. The two measures, ingestive and aversive responding, were obtained by recording the rat's reactions to the stimuli as they were infused directly into the oral cavity. This taste reactivity method both enabled us to use avoided stimuli in a nondeprived animal and to measure the rat's evaluation of the stimuli's aversiveness. Problems with stimulus sampling may be responsible for the dearth of conditioning experiments which utilize avoided tastes in conditioned preference studies.

Animals↗

Applications of taste reactivity to the study of the neural-hormonal controls of ingestive behavior.

Taste plays a central role in guiding ingestive behavior and the encoding of taste is affected by manipulations that influence ingestive behavior. In this article, the use of the taste reactivity test to provide a behavioral assessment of how changes in the oral reinforcing properties of a taste may initiate or sustain ingestive behaviors in several contexts are discussed. The affects of the animal's sex, sodium deficiency, exogenous bombesin administration, and the role of central gustatory lesions in mediating taste reactivity responses are discussed. Findings indicate that an enhancement of ingestive taste reactivity responses correlate with an increased preference and intake of taste stimuli for some, but not all situations. Such situations include the bombesin-like peptides that reduce sucrose and sodium chloride intake without influencing taste reactivity responses. Conversely, female rats, compared to males, show an elevated intake and preference for a range of NaCl concentrations and a greater number of ingestive taste reactivity responses to some, but not all of the preferred concentrations. Such mismatches of taste reactivity and intake measures shift attention to the contribution of nongustatory factors (trigeminal, visceral) in the control of intake.

Animals↗