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In two groups of 15-year-olds--50 with a high and 50 with a low caries experience--recognition thresholds were determined for sweet, salty, sour, and bitter tastes and preferences for sweet taste, using a full-mouth technique. No statistically significant difference in thresholds could be found between the groups. No correlation between threshold values and preferences for sucrose could be established.
Behavioral and electrophysiological experiments were performed to examine whether or not the taste of 'umami' substances such as monosodium glutamate (MSG), disodium 5'-inosinate (IMP), and disodium 5'-guanilate (GMP) is really unique in hamsters. When the animals were conditioned to avoid ingestion of MSG (or IMP) or their mixture by pairing its ingestion with an i.p. injection of LiCl, suppression of drinking generalized to IMP (or MSG), GMP, NaCl, and other sodium salts. Suppression of drinking after conditioning to NaCl generalized to MSG, IMP, GMP, and inorganic sodium salts. These learned aversions to umami substances and sodium salts were abolished by bilateral deafferentation of the chorda tympani, but were not affected by destruction of the bilateral glossopharyngeal nerves. The integrated whole-nerve responses of the chorda tympani to MSG, IMP, and NaCl were similar to each other, consisting of the initial dynamic phase and the following tonic phase. Synergism of chorda tympani responses to a mixture of MSG and IMP was not observed. Across-fiber response patterns of the chorda tympani for MSG, IMP, or their mixture were very similar to that for NaCl. Even the high concentrations of umami substances (0.3 M MSG, 0.3 M IMP, and the mixture) did not elicit any detectable responses in the glossopharyngeal nerve. These results suggest that the taste of umami substances is not unique in the hamster, but is similar to that of sodium salts, and is mediated exclusively via the chorda tympani.
Epithelial tissues and papilla from several regions of the steer tongue were isolated and the fatty acids from each lipid class in the polar and neutral fractions were assayed. The observed profiles indicated regional differences. Arachidonic acid and other fatty acids containing long carbon chains (greater than 22) were found in all tissues sampled, particularly in the phosphatidyls of the inositols, ethanolamines, cholines, and in the cholesterylesters. Production of prostaglandin E2 was measured through cyclo-oxygenase activity and the presence of plasmalogens was observed in the phosphatidylethanolamine and choline fractions. Higher rates of PGE2 synthesis and greater amounts of plasmologens were found in taste-related epithelial samples compared to lingual epithelial control samples not containing taste buds. The heterogeneity of patterns of lipids and fatty acids found in the epithelium of the tongue suggests possible zonal specialization to satisfy regional physiological needs.
The ability of rats to make intensity discriminations was determined by forming a conditioned taste aversion to a moderate concentration of each of four basic taste stimuli, and then measuring the level of acceptance (number of licks during a 15 sec exposure) shown to a range of concentrations of the same chemical. Rats (N = 66) could discriminate between glucose concentrations that were separated by as little as 0.074 M, between NaCl concentrations that differed by 0.029 M, between HCl concentrations that were 9 X 10(-4) M apart, and between quinine HCl concentrations that differed by as little as 2.4 X 10(-6) M.
In order to confirm the effect of umami taste stimulation on visceral functions, blood insulin and glucose assays and an electrophysiological study were performed on the rat. Blood insulin and glucose assays were carried out in conscious and free-moving rats. When the oral cavity was infused by MSG solution, a transient increase in blood insulin level was recognized at 3 min after this oral stimulation. The electrophysiological study revealed that applications of monosodium glutamate (MSG) glucose to the tongue in the anesthetized rat caused an increase in efferent activity of the pancreatic branch of the vagus nerve. These observations support the conclusion that taste stimulation of MSG induces cephalic-phase insulin secretion.
Inhalation by rats of nitrous oxide immediately after ingestion of a solution of 0.1% saccharin resulted in a conditioned avoidance of the solution following recovery from the drug (Conditioned Taste Aversion). With a constant duration of inhalation (30 min), aversive properties of nitrous oxide in this behavioural paradigm were related to concentration over the range 0-80%. At constant concentrations (70% and 80%), the aversive potency of nitrous oxide was directly related to duration of inhalation of the gas over the range 0-4 hr. These data provide the first direct support for the hypothesis [5,6] that a major determinant of aversive potency of a drug in the taste aversion paradigm is its duration of action. Different temporal components of drug action may mediate self-administration and conditioned aversion.
The concept of four primary tastes has been used to direct research and organize data in gustation. The attractive simplicity of this formulation has directed attention away from critical examinations of its validity. The present article shows that arguments used to support the concept of four tastes are equivocal. It is also suggested that the data are more consistent with the hypothesis that gustatory data have a more continuous organization which includes the familial primary four. Data are considered at the stimulus, receptor, neural, and psychophysical levels.
Previous studies (V. J. Djurić, B. M. Marković, M. Lazarević, & B. D. Janković, 1987, in B. D. Janković, B. M. Marković, & N. H. Spector (Eds.), Neuroimmune interactions, pp. 561-568, New York: New York Acad. Sci.; B. M. Marković, V. J. Djurić, M. Lazarević, & B. D. Janković, 1988, Brain Behav. Immun. 2, 11-23) have shown that rats learn to associate the taste of saccharin with the induction of anaphylactic shock, thus exhibiting conditioned taste aversion (CTA) toward an otherwise preferred saccharin solution. The present experiment investigates the effect of unconditioned stimulus intensity (the amount of antigen used for the induction of shock) on CTA. Rats were sensitized to ovalbumin and subjected to a conditioning trial in which the conditioned stimulus (CS; saccharin solution given orally) signaled the presentation of the unconditioned stimulus (US; shocking doses of ovalbumin ranging from 0.5 to 3 mg given intraperitoneally). Behavioral signs, hematocrit, and rectal temperature were used for evaluation of anaphylactic shock. Twenty-four hours after the conditioning trial, rats were subjected to a two-bottle preference test between saccharin solution and water. Multiple regression statistical analysis revealed significant correlations among saccharin preference ratio, dose of antigen used for the induction of shock, behavioral signs of shock, rise in hematocrit, and fall in rectal temperature. A dose-dependent relation among saccharin preference ratio and physiological indicators of shock suggests that conditioned anaphylactic shock-induced avoidance behavior is functionally related to homeostatic factors involved in immune reactivity.
BACKGROUND: The interactions among experience, emotion, and memory are considered to be instrumental in the ontogeny and maintenance of acquired emotional and behavioral disorders (e.g., phobias). Here we address the question whether an anxiety-like state can associate with taste to produce conditioned taste aversion (CTA). METHODS: We have used an anxiogenic agent, the 5-HT2C receptor agonist meta-chlorophenylpiperazine (mCPP), to induce an anxiety-like emotional state in rats after consumption of an unfamiliar tastant. RESULTS: The anxiogenic agent induced CTA. The mCPP-induced CTA could be prevented by concomitant administration of ethanol, which is known to reverse mCPP-induced anxiety-like behavior, at a concentration that had no effect on CTA memory. In contrast, ethanol did not prevent LiCl-induced CTA. Administration of mCPP before the consumption of the tastant had no effect on the preference for that tastant. CONCLUSIONS: Taken together, these results indicate that anxiety-like state can serve as the unconditioned stimulus in CTA training. This finding may be relevant to the ontogeny of pathologies involving food aversion.
Recent studies of taste receptors in Drosophila show remarkable parallels with the mammalian gustatory system, although the pathways are anatomically distinct. These parallels may reflect crucial constraints in the design of taste detection systems.
The conditioned taste aversion (CTA) threshold for either citric acid (CA) or HCl solutions and the two-bottle taste preference (TBP) threshold were determined in rats that are familiarized to the odor of conditioning solutions or that are naive. The CTA method appeared to be more sensitive than the TBP test, particularly when rats were not familiarized to the odor of the conditioning solution. The CTA threshold for HCl-conditioned rats and familiarized to the odor of conditioning solution lies between 1.00 and 2.00 mmol; in unconditioned rats, it lies between 4.00 and 5.00 mmol. In CA-conditioned and odor-familiarized rats, the threshold lies between 0.09 and 0.20 mmol; in unconditioned rats, it lies between 7.00 and 10.00 mmol. In rats not familiarized to the odor of the conditioning solution, the threshold for HCl-conditioned rats lies between 0.90 and 1.00 mmol; in unconditioned rats, it lies between 2.00 and 3.00 mmol. In CA-conditioned rats, the CTA threshold lies between 0.03 and 0.05 mmol; in unconditioned rats, it lies between 4.00 and 7.00 mmol. The two-bottle test is less sensitive than the CTA method. The TBP threshold lies between HCl 4.00 and 5.00 mmol, and between CA 4.00 and 7.00 mmol. The odor of a solution may potentiate the ability of rats to detect the concentration of CA and HCl solutions.
Chicks (n = 208) received CS solutions of red water, red 2.0% vinegar, clear water, or clear 2.0% vinegar, followed by an I.P. injection of 0.4 M lithium chloride at 0.2% or 0.5% body weight, and then received 2 test trials with red water or clear 2.0% vinegar. In testing with red water, measures of latency to start drinking, latency to make 9 more drinks after the first, and amount drunk provided reliable evidence of potentiated aversion to visual cues with a greater magnitude of potentiation shown following the 0.2% injection than the 0.5% injection. In testing with clear vinegar, the "9-drink" latency measure and amount drunk yielded reliable evidence of taste aversion, with greater aversion shown following the 0.5% injection than the 0.2% injection. Findings are discussed in terms of associative and taste primacy views of potentiation effects.
Umami substances such as monopotassium L-glutamate (MPG) and 5'-inosine monophosphate (IMP) elicit a unique taste called 'umami' in humans. To elucidate the umami receptor mechanism in rats, we examined taste responses of the chorda tympani nerve by using three ionotropic glutamate receptor agonists, NMDA, KA and AMPA, a mGluR4 agonist, L-AP4, and a specific mGluR4 antagonist, MAP4, and an anti-sweet peptide, gurmarin. When IMP was added, synergistic responses were shown only for MPG and L-AP4, but not for NMDA, KA and AMPA. MAP4 enhanced the responses to MPG and L-AP4. Gurmarin suppressed the synergistic responses to mixtures of MPG and IMP or L-AP4 and IMP. These results suggest that glutamate and L-AP4 bind both the sweet-responsive macromolecule and mGluR4, but the synergism occurs only on the macromolecule.
Taste responses to fructose and tannic acid were compared between great apes using the 'two-bottle test' with tests of brief duration. The taste thresholds for fructose were [10-20] mM in Pongo pygmaeus, [40-50] mM in Pan troglodytes, and [70-80] mM in Gorilla gorilla. Inhibition thresholds for tannic acid were [2.9-3.5] mM in Pongo and [2.9-5.9] mM in Pan. Gorillas apparently significantly preferred tannins at low concentrations ([0.59-5.9] mM) but rejected concentrations above [8.8-14.7] mM. These results are discussed in relation to the effects of phylogenetic inertia and biological adaptation.
The anterior insular gustatory neocortex (AIGN) has been implicated as a functional substrate of conditioned taste aversion (CTA) learning. Results of previous neuroanatomical and neurobehavioral experiments indicate that projections from gustatory-responsive neurons in the posterior ventromedial thalamic nuclei (parvicellular division; VPMpc) may provide relevant input to the AIGN during CTA learning. In rat, gustatory thalamocortical projections from VPMpc thalamus traverse the ventrolateral neostriatum (VLS) enroute to the AIGN. In these experiments, various neuroanatomical and neurobehavioral manipulations in the VLS were used to examine the contribution of presumed gustatory thalamocortical projections to CTA learning. These experiments demonstrate that projections from VPMpc thalamus to the AIGN are essential for normal CTA learning. Because both VPMpc thalamus and the AIGN each have been implicated as functional substrates of CTA learning, the present results suggest that the gustatory thalamocortical relay per se is necessary for normal taste-illness learning.
Fibers of the frog glossopharyngeal nerve (water fibers) that are sensitive to water also respond to CaCl2, MgCl2 and NaCl. In the present study, interaction among cations (Ca2+, Mg2+ and Na+) on taste cell membrane in frogs was studied using transition metals (NiCl2, CoCl2 and MnCl2), which themselves are barely effective in producing neural response at concentrations below 5 mM. Unitary discharges from single water fibers were recorded from fungiform papillae with suction electrode. Transition metal ions (0.05-5.0 mM) had exclusively enhancing effects on the responses to 50 mM Ca2+, 100 mM Mg2+ and 500 mM Na+. The effects of transition metal ions were always reversible. The rank order of effectiveness of transition metals at 1 mM in the enhancement of the responses to 50 mM CaCl2, 100 mM MgCl2 and 500 mM NaCl was NiCl2 > CoCl2 > MnCl2. The concentration of transition metal ions effective to enhance salt response was almost the same among Ca2+, Mg2+ and Na+ responses. The results suggest that a common mechanism is involved in the enhancement of Ca2+, Mg2+ and Na+ taste responses. The enhanced Mg2+ response and the enhanced Na+ response were greatly inhibited by the addition of Ca2+ ions, and the enhanced Ca2+ response was inhibited by the addition of Mg2+ or Na+ ions, suggesting that competitive antagonism occurs between Ca2+ and Mg2+ ions and between Ca2+ and Na+ ions in the presence of Ni2+ ions. Ni2+ ions had a dual effect on the Ca2+ response induced by low concentration (0.1 mM) of CaCl2: enhancement at lower concentrations (0.02-0.1 mM) of NiCl2 and inhibition at higher concentrations (0.5-5 mM) of NiCl2. The present results suggest that transition metal ions do not affect the receptor-antagonist complex, but affect only the receptor-agonist complex.
Bitter taste thresholds for 6-n-propylthiouracil are bimodally distributed, dividing subjects into tasters and nontasters. Their taste worlds differ with regard to the sweetness of sucrose and saccharin and to the bitterness of saccharin. These differences suggest that nontasters tend to perceive less bitterness in saccharin at concentrations used in beverages.
Changes in the luminal contents of the gastrointestinal tract modulate gastrointestinal functions, including absorption of nutrients, food intake, and protection against harmful substances. The current notion is that mucosal enteroendocrine cells act as primary chemoreceptors by releasing signaling molecules in response to changes in the luminal environment, which in turn activate nerve terminals. The recent discovery that taste receptors and G protein subunits alpha-gustducin and alpha-transducin, involved in gustatory signal transduction, are expressed in the gastrointestinal mucosa supports the concept of a chemosensory machinery in the gastrointestinal tract. An understanding of luminal sensing processes responsible for the generation of the appropriate functional response to specific nutrients and nonnutrients is of clinical importance since aberrant or unsteady responses to changes in luminal contents might result in disease states ranging from intoxication to feeding disorders and inflammation. The purpose of this theme article is to discuss the functional implications of bitter taste signaling molecules in the gastrointestinal tract deduced by their localization in selected populations of epithelial cells and their relationship with neural pathways responsible for the generation of specific responses to luminal contents.