An assessment of alginate materials.
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The study of learning and memory using the chicken model has relied on three learning paradigms, passive avoidance learning, imprinting and the pebble floor task. Passive avoidance learning and imprinting have been used predominantly in very young chickens and cannot be used to access learning and memory in older chickens. We have established a new behavioural learning paradigm, Discriminative Taste Aversion Learning (DTAL), that can be used with both young and older animals. The task requires chickens to discriminate between food crumbs dyed either red or yellow with one colour being associated with the aversive tasting substance, methylanthranilate. Learning can be tested at various times after the training session by presenting chickens with the coloured food crumbs without an aversive taste. Both chickens tested at 5 and 15 days post-hatch learned to avoid the aversive crumbs. Furthermore, the protein synthesis inhibitor anisomycin (30 mM; 10 microl per hemisphere) injected into the intermediate medial hyperstriatum ventrale 15 min pre-training or 45 min post-training blocked long-term memory for the DTAL task when tested 24 h later. Memory for the task was unaffected by anisomycin injection 120 min post-training or in control animals injected with saline at similar times. The timing of the cellular processes of protein synthesis needed for consolidation of the DTAL appears to be similar to those described for the other behavioural paradigms in young chickens.
Rats injected with lithium chloride after exposure to a taste or olfactory stimulus learn stronger aversions to these cues if the drug is administered in two small injections 35 min apart than if all of the drug is given in a single injection. This facilitation of conditioning produced by distribution of the drug unconditioned stimulus occurs with both low and high lithium doses (Experiments 1 and 2), is more evident in male than in female rats (Experiment 1), and is directly related to the amount of the flavored solution consumed prior to drug treatment (Experiment 4). Increasing the interval between two small drug injections beyond an optimal value results in a progressive loss of the facilitation of conditioning (Experiments 2 and 3), and the optimal drug distribution interval may be shorter for olfactory cues (Experiment 3) than for taste stimuli (Experiments 1 and 2). Control observations (Experiments 5A and 5B) showed that the drug distribution effect is not due to handling or other non-drug factors involved in giving two rather than only one injection. The phenomenon is consistent with recently-proposed models of conditioning and suggests that the differential effectiveness of various drugs in taste aversion conditioning may be related to differences in the time course of the unconditioned drug effects.
With the use of Corey-Pauling -Koltun space-filling models, measurements of defined parameters (x, y, and z) were made of the R groups in a large number of carbosulfamates, RNHSO-3. The correlation between sweet and nonsweet sulfamates and the defined parameters for R is good. As a test, 12 new carbosulfamates were synthesized and tasted. The predictions of their sweetness or nonsweetness based on the correlation were greater than 90% correct. To elicit a sweet taste, the R group of the sulfamate should have x greater than or equal to 5.2 A and less than or equal to 7.2 A and V (i.e.,xyz) less than or equal to 250 A3 and probably greater than or equal to 90 A3. The receptor site is seen (as for aspartame) as a rather narrow cleft into which R has to fit "properly" or be "locked" so that the AH,B mechanism for initiating the sweet stimulae can operate. Possible applications of this approach are indicated.
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The active sites of the receptors for sweet and bitter tastants are shown to be related by a simple symmetry operation. This relationship, in turn, allows the identification of the critical geometrical features of both receptor sites. The model proposed for the sweet site is shown to be consistent with a large number of (conformationally rigid) sweet molecules.
BACKGROUND: Research on risk factors for premenstrual syndrome (PMS) is lacking for the Gulf countries of the Middle East, a region with unique cultural features that might influence expectations and self-perception of the disease. We examined the association of PMS frequency with possible risk factors for the disease. METHODS: Using a self-report questionnaire, we surveyed all eligible young women (n=464) enrolled in the medical, nursing and medical technology/respiratory therapy educational programs at a university in Dammam. Women were asked about the frequency of symptoms during the previous six months. A stepwise multiple regression analysis was performed to determine which of several biopsychosocial and dietary factors influenced the premenstrual symptom score. RESULTS: At least one premenstrual symptom was experienced by 448 women (96.6%), and 176 (37.5%) had a high symptom severity score. Premenstrual symptom frequency was significantly associated with a maternal history of premenstrual syndrome, self-perception of mental stress, physical activity, consumption of sweet-tasting foods, and coffee, but these factors only explained 14% of the variability in the multiple regression model. CONCLUSIONS: We recommend that women vulnerable to mental stress take advantage of relaxation techniques and psychotropic therapies. Moreover, women with PMS might eliminate sweet-tasting food and caffeine-containing beverages, particularly coffee, from their diet.
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Sensitivity to the bitter acetylated sugar sucrose octaacetate (SOA) is mediated by a single-locus system with three alleles in mice. Inbred strains are classified according to SOA phenotype as tasters, nontasters, or demitasters (intermediate sensitivity). A congenic quartet created from taster and nontaster strains has been used to investigate the effect of the Soa locus on non-SOA aspects of taste sensitivity. In this study, we created a third congenic set, C3.SW-Soaa, from taster (SWR/J) and demitaster (C3HeB/FeJ) strains. After 11 lineal backcross generations these C3.SW mice carry the tasting allele on a 99% C3 demitaster background. After testing a total of 938 mice, taster-demitaster proportions across 12 generations were consistent with expectations from a monogenic model. The resultant three-strain congenic series will allow further examination of the mechanisms of taste.
Rats are protected against intake of toxic diets by specific evolutionary prepared behavioral adaptations. Intake of potentially dangerous novel food is reduced by neophobia. The taste signal is stored for several hours in a short-term memory file from which it gradually emerges in form of a permanent gustatory engram labeled as safe, when there are no adverse effects of feeding, or as aversive, when visceral symptoms of poisoning appear in the critical post-ingestion interval. The experimental evidence reviewed indicates that positive labeling (manifested by attenuation of neophobia) requires intact higher brain functions whereas the aversive experience (manifested by conditioned taste aversion) is recorded even under deep coma. The biological significance of the different neural mechanisms underlying the above forms of gustatory-visceral associations is discussed.
RATIONALE: Previous studies have shown that GIRK2 channel function is enhanced by ethanol and that GIRK2 null mutant mice are less sensitive to some of ethanol's effects, including anxiolysis, habituated locomotor stimulation, and acute handling-induced convulsions than wild types. Under some conditions, GIRK2 knockout mice consume more ethanol than wild types, but it is unclear whether they do so because they are more sensitive to ethanol's rewarding effects or less sensitive to its aversive effects. OBJECTIVE: To further assess the role of GIRK2 in ethanol action, GIRK2 null mutant and wild type mice were tested in conditioning models that measure the motivational effects of ethanol. METHOD: In a conditioned taste aversion (CTA) procedure, knockout and wild type mice were given ethanol (0.0, 2.0, 2.5, or 3.5 g/kg, IP) following 1-h access to saccharin every 48 h over a 10 day period. In a conditioned place preference (CPP) procedure, knockout and wild type mice were given ethanol (2.0 or 3.0 g/kg, IP) paired with one stimulus (grid or hole floor) and saline paired with the other. After four 5-min trials with each stimulus, a 60-min choice test was done. RESULTS: The results demonstrated a genotypic difference in both paradigms. In CTA, there was no difference between genotypes at 0.0 or 3.5 g/kg ethanol, but at the 2.0 and 2.5 g/kg doses, wild types developed a stronger aversion to saccharin than knockouts. In CPP, wild types developed place preference, but knockouts did not. CONCLUSIONS: These studies show that GIRK2 deletion reduced ethanol's impact in tasks that are commonly used to index the drug's rewarding and aversive effects. These findings could reflect either a learning/memory deficit or decreased sensitivity to ethanol's motivational effects in null mutant mice. The latter interpretation is more consistent with previous data showing that knockout mice consume higher doses of ethanol than wild type mice.
Responses to a 5-min anoxia were studied in cats with different taste sensitivity for phenilthiocarbamide (PTC). The sensitive animals were more resistant against hypoxia. The difference in the cats seems to be determined by the condition of the cAMP system involved in adaptive responses.
After gastrulation, the pharyngeal endoderm is specified to give rise to taste receptor organs without further signaling from other embryonic tissues. We hypothesized that intercellular signaling might be responsible for the specification of taste buds. To test if and when this signaling was occurring, intercellular contacts were transiently disrupted in cultures of pharyngeal endoderm from axolotl embryos, and the number, size, and distribution of taste buds analyzed. Disruption of cell contacts at progressive time points, from neurula to late tail bud stages, revealed a critical period, during mid-tail bud stages, when disruption of cell contacts resulted in a significant increase in taste bud number and size. The spatial distribution of taste buds was also altered; taste buds were more clustered in explants disrupted during the critical period. These effects were not due to general alterations in mitosis and apoptosis. Rather, at least three aspects of taste bud patterning, i.e., number, size, and distribution, are governed by mechanisms dependent on normal cell contacts during a concise time window. Furthermore, our findings are consistent with specification of taste buds by means of lateral inhibitory signaling, which we hypothesize results from cell contact-dependent or short-range diffusible signals.
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