Influence of housing conditions and state of partner on conditioning and extinction of taste aversion to lithium and chlorpromazine

Rats were used in two experiments to investigate the influence of social variables on the acquisition of Conditioned Taste Aversion (CTA) to either lithium chloride (10 ml/kg IP of a 0.3-M solution given twice) or chlorpromazine (8 mg/kg IP given four times) and on subsequent extinction. CTA acquisition was not affected by original housing assignment (isolation or paired housing for 15–23 days prior to conditioning), by the shifted social assignment during conditioning, or by the drugged state of the paired animals' partners on drug-scheduled days. However, for both drugs, permanently isolated animals extinguished CTA more slowly than rats housed permanently in pairs. Shifts from isolation to pairing or vice versa failed to alter CTA extinction in the case of lithium, but affected it significantly in chlorpromazine-treated rats. Shifts from isolation to paired housing with an undrugged partner produced faster extinction for lithium than the corresponding group with a drugged partner. For chlorpromazine, the effect of the same shift was exactly the opposite. Overall, the results show that changes in CTA extinction can be a function of social variables.     

Effects of dorsolateral tegmental lesions on amphetamine- and lithium-induced taste aversions

Female rats with lesions of the dorsolateral tegmentum (DLT) displayed both hyperphagia and attenuation of the conditioned taste aversion induced by amphetamine (2.0 mg/kg). DLT lesions, however, did not influence conditioned taste aversion induced by lithium chloride (0.15 M). These outcomes complement recent observations of attenuated lithium, but not amphetamine, taste aversion following destruction of the area postrema. It is suggested that the ventral nonadrenergic bundle, at the level of the dorsolateral tegmentum, may mediate the aversive properties of amphetamine.     

Ethanol-Induced Conditioned Taste Aversion in BXD Recombinant Inbred Mice

Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, ip). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9,11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the 6 opioid receptor, and two serotonin receptors (lB and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2,3,4,6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.     

Three-dimensional structure of the gustatory cell in the mouse fungiform taste buds: a computer-assisted reconstruction from serial ultrathin sections

Taste buds in fungiform papillae of the mouse were examined with transmission electron microscopy and computer-assisted, three-dimensional reconstructions from serial ultrathin sections. In accord with observation by Murray (1971), four distinct cell types, type I, II, III and basal cells, were identified. Of these, only the type III cell made synaptic contacts with nerve terminals and contained both small, clear vesicles and dense-cored granules. The former vesicles were synaptic-type and accumulated in the cytoplasm just below the synaptic in membrane thickenings. This finding clearly indicates a sensory function for the type III cell. One to three type III cells were identified within a taste bud. The type III cell had at most eight synapses with nerve terminals. One nerve fiber making two synapses with the type III cell was occasionally observed in its terminal region.     

Selective suppression of judged sweetness by ziziphins

The effects of ziziphins and of control treatments upon judgments by human adults of the sweetness, sourness, bitterness, and saltiness of American apple cider or apple juice were measured with a category estimation method during repeated trials before, during (90 sec treatment duration only), and after, treatment. Sweetness was reduced after either a 10 sec or a 90 sec whole mouth treatment with ziziphins, but not after quinine sulfate or apple juice control treatment. No differences in after-treatment sourness, bitterness, or saltiness occurred between treatments. The reduction in sweetness was weak with 10 sec 3.5% W/V ziziphins treatment, but strong after 90 sec 0.88% W/V ziziphins treatment; duration of suppression was ca. 70 sec. The mechanism was identified as taste modification since adaptation, cross-adaptation, and mixture suppression were eliminated by control treatments and by post-treatment rests and rinse. Comparisons with known gumnemic acids effects suggest that net dissociation of ziziphins from taste receptor membranes and/or inactivation in the membrane may be much faster than with gymnemic acids.     

Ovariectomy fails to affect rats' quinine aversion

Three studies investigated the effects of ovariectomy on the intake of quinine solutions. Despite significant elevations of body weight due to surgery, no change in quinine preference was noted. Varying the age of surgery (prepuberty, postpuberty, and adulthood), age of testing, and time between these events did not alter the basic findings.     

The issue of primary tastes versus a taste continuum

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 familiar primary four. Data are considered at the stimulus, receptor, neural, and psychophysical levels.     

Gonadal hormones and behavioral regulation of body weight

Gonadal hormones have important effects on the behaviors that determine body weight in laboratory rats (i.e., eating, locomotor activity, and thermoregulatory behavior). These effects are most evident in the female where there are consistent, predictable changes in these behaviors which are correlated with fluctuations in plasma hormone levels during estrous cycles, puberty, pregnancy, or after gonadectomy and replacement therapy. Estradiol, which seems to be the principal ovarian steroid affecting body weight, may act directly on separate neural loci to: (a) inhibit food intake and (b) stimulate locomotor activity, possibly by lowering the set-point of a hypothalamic lipostat. Estradiol does not affect eating and running in prepubertal female rats, perhaps because of influences of pituitary hormone(s) at this age. Ovarian hormones also alter the taste preferences of rats and may be responsible for the changes in self-selection of dietary components during different reproductive states. Some implications of this research are discussed and possible directions for future research suggested.     

Reduction of learned taste aversions by pre-exposure to drugs

Taste aversions are induced by a variety of psychotropic drugs. In the present experiments taste aversions induced by the barbiturate hypnotic drug, amobarbital, were dramatically reduced by prior exposure to the drug. Increasing numbers of pre-exposures were associated with larger reductions in taste aversions. Reductions in sleeping time (a widely accepted measure of tolerance to barbiturate drugs) were not correlated with reductions in taste aversions. Taste aversions induced by amobarbital were also impaired following pre-exposure to the pharmacologically dissimilar drug d-amphetamine. These results suggest that reduced taste aversions following pre-exposure to drugs may reflect habituation to drug-related stimuli and not solely the development of tolerance to those drugs.Presented in part to the Psychonomic Society, Boston, 1974.     

Using profiles of saccharin and water drinking to detect and discriminate actions of drugs and toxicants

Experiments were conducted to investigate the feasibility of using the pattern of saccharin and water drinking to detect acute and chronic administration of drugs and toxicants. Procedural variables were found to be crucial. When rats were naive for the saccharin drinking fluid, a single injection of LiCl or 2-deoxyglucose produced persistant saccharin aversion. Hypertonic saline produced only a transient saccharin aversion. If rats were pre-exposed to saccharin, the 2-deoxyglucose injection and hypertonic NaCl produced an increase in saccharin drinking but LiCl was without effect. Several types of chronic treatment were given to saccharin-experienced rats. Chronic 2-deoxyglucose, LiCl, and Pb administration produced gradually developing saccharin aversion and qualitatively different patterns of saccharin and water drinking. Chronic administration of hypertonic NaCl or insulin or chronic food deprivation had no impact on saccharin preference. It was concluded that patterns of saccharin and water drinking can be used to detect the administration of a drug or toxicant and perhaps even the time course of action, but may not detect a substance given previous to saccharin, perhaps because the animal cannot associate these now familiar perturbations with the novel saccharin solution. This means that existing toxic states may not be detected by using saccharin preference as a probe.