Microinjections of dopaminergic agents in the nucleus accumbens affect ethanol consumption but not palatability.

It was determined whether ethanol palatability in rats could be changed by manipulating the reinforcement experienced during limited access consumption. During the first 3 days of the experiment, initial taste reactivity (TR) testing to distilled water (1 day) and 10% alcohol (2 days) was performed. Following the establishment of baseline TR, separate groups of animals received bilateral microinjections (0.5 microl/side) into the nucleus accumbens of either the nonspecific dopamine agonist d-amphetamine sulfate (20 microg, n = 10), the D(2) antagonist raclopride (1.0 microg, n = 8), or physiological saline (n = 5). The injections occurred at the same time each day for 5 consecutive days. Five minutes after the microinjection, the fluid-deprived rats were given 30-min access to 10% ethanol. Over the 3 days following drug administration, TR to distilled water and 10% alcohol was repeated. After this, the rats were once again given 30 min of access to 10% ethanol for 5 consecutive days, but without drug microinjection prior to alcohol access. A final TR exposure (the same as the others) was performed over the final 3 days of the study. Both raclopride and d-amphetamine administration produced reductions in ethanol consumption (in comparison to saline treatment). However, treatment with d-amphetamine and raclopride during ethanol consumption did not cause significant, conditioned changes in palatability as measured by the taste reactivity procedure. These results suggest that dopamine plays a role in the motivation to consume ethanol but this neurotransmitter is not involved in evaluating its incentive value.

Taste reactivity in alcohol-preferring AA and alcohol-avoiding ANA rats.

Alcohol-preferring rats (Alko alcohol or AA) were tested for taste reactivity to water, sucrose, quinine, and a range of alcohol concentrations (5-40%) both before and after a period of continuous alcohol access. The alcohol-avoiding line of rats (Alko nonalcohol or ANA) was also tested for comparison. It was found that AA rats displayed greater ingestive reactivity to alcohol compared to ANA rats both before and after a three-week period of continuous access to 10% alcohol (during which time AA rats drank significantly more alcohol than ANA rats). AA rats also made significantly more ingestive responses to a 0.3 M sucrose solution and a 0.0005 M quinine solution. Differences between AA rats and ANA rats in aversive reactivity appeared only after the alcohol consumption tests; AA rats made significantly fewer aversive responses to the 30% and 40% concentrations after continuous alcohol access. AA rats also made significantly more aversive responses to the quinine solution. The results suggest that line differences between AA rats and ANA rats in the reactivity response to alcohol solutions have been selected in association with the original selection phenotype of alcohol consumption.

Ethanol consumption in rats selectively bred for differential saccharin intake.

Rat lines selectively bred for high ethanol consumption consume more saccharin solution than do their low-ethanol-consuming counterparts. The present study utilized the technique of reciprocal selection to examine the reliability of the saccharin/ethanol relationship; specifically, consumption of 1-10% ethanol solution was measured in rats selectively bred for high vs. low saccharin consumption (Occidental HiS and LoS lines). HiS rats consumed more ethanol than did LoS rats. These results support the idea that individual differences in ethanol and saccharin consumption share some common mechanism(s).

Taste reactivity to alcohol and basic tastes in outbred mice.

The taste reactivity test was used to determine the response of outbred mice to orally infused taste solutions. For the initial measures, mice (n = 10) were tested with 3%, 6%, 9%, and 12% (v/v) alcohol and four taste solutions: sucrose, sodium chloride, hydrochloric acid, and quinine hydrochloride (a single concentration of each). A second group of naive mice (n = 16) was tested with 5%, 10%, 20%, 30%, and 40% alcohol. The final set of measures with naive mice (n = 26) was taken with a range of sucrose concentrations: 0.01 M, 0.05 M, 0.1 M, 0.5 M, and 1.0 M. In general, mice made similar reactivity responses to all solutions tested. A predominant component of the mouse response to all infused fluids was forelimb flailing; gaping was also a common response to all solutions. Despite the large number of aversive-type responses, mice rejected very little fluid via passive drip or fluid expulsion. The single, significant difference in responding to the four taste stimuli was that mice made fewer aversive responses to sucrose. Differential responding to the 5 to 40% alcohol concentrations and sucrose concentrations was observed. Mice increased ingestive responding as the concentration of alcohol and sucrose increased. Aversive responding decreased reliably only with increases in the sucrose concentration. Data provide the first reported taste reactivity responses of mice to orally infused taste solutions. These results can be compared with the extant data available in rats and can also be used as a basis for exploring taste factors in genetically defined mouse populations.

Naltrexone treatment increases the aversiveness of alcohol for outbred rats.

Acute naltrexone treatments (0.0, 0.5, 1., or 3.0 mg/kg body weight) were administered to separate groups of rats and alcohol taste reactivity and consumption were measured. Rats were given daily naltrexone injections and then tested for taste reactivity to 10% alcohol 30 and 60 min after injection. Each reactivity trial (total of 4) was 60 sec during which 1 ml of fluid was infused. The rats' orofacial and body movements were videotaped and scored later. In the final measure, rats were placed on a restricted fluid access schedule and given naltrexone treatments 10 min before being presented with the 10% alcohol solution in the home case (60-min drinking period). After 4 days of consumption tests under the drug condition, the rats were given 4 more daily tests without the drug. Results indicated that the two highest naltrexone doses significantly decreased ingestive responding and increased aversive responding, particularly at the 30-min test. Both the 1.0 and 3.0 mg/kg body weight doses also significantly decreased alcohol consumption as measured during the free access tests. Alcohol consumption returned to control levels immediately after the drug treatments were stopped. The data show that dosages of naltrexone 1.0 mg or higher significantly alter both alcohol taste reactivity (increased aversiveness and decreased palatability) and alcohol consumption (decreased intake) in outbred rats. These results are discussed in relation to naltrexone treatment as a means for decreasing alcohol use and abuse.

Taste reactivity in high-alcohol-sensitive and low-alcohol-sensitive rats.

High, low, and control alcohol-sensitive (HAS, LAS, CAS, respectively) rats were tested for their perception of the taste of alcohol using the taste reactivity test. Reactivity tests with a single concentration of sucrose and quinine were also done. After initial taste reactivity, all rats were tested for alcohol consumption in a standard two-bottle test (water in the second bottle). Postconsumption taste reactivity tests completed the experiment. Results indicated that HAS, LAS, and CAS rats did not differ significantly in their taste reactivity response to a range of alcohol concentrations (5-40%), nor did they differ significantly in response to sucrose or quinine. Reactivity responses were similar for each group before and after the consumption tests. Despite the lack of line differences in taste reactivity, HAS and LAS rats consumed significantly less alcohol than the CAS rats during the two-bottle access tests. The present results are in contrast to research done with rats selectively bred for alcohol consumption (Alcohol Preferring and Nonpreferring rats, High Alcohol Drinking and Low Alcohol Drinking rats), which exhibit clear line differences in patterns of reactivity changes following alcohol access. The selection phenotype of alcohol sensitivity appears to be independent of rats' behavioral response to the taste of alcohol.

Continuous intraoral saccharin infusions in high vs. low saccharin-consuming rats.

Confirmed high saccharin (HiS)-consuming and low saccharin (LoS)-consuming rats were compared in their taste response to saccharin using a continuous intraoral infusion procedure. On 2 separate days, rats were infused with 0.1% saccharin (rate = 1 ml/min) until they rejected fluid via passive drip or forceful fluid expulsion (at which time infusion was stopped for 30 s), and then again rejected fluid within 30 s after infusion was reinitiated. Two dependent measures were collected during infusion procedures: latency to first fluid rejection and total infusion time. On the first infusion day, HiS and LoS rats produced similar latencies to first rejection and total infusion times. However, HiS rats displayed significantly longer latencies to first rejection than LoS rats on the second infusion day. The results indicate that continuous infusion procedures exposed differences between HiS and LoS lines, but only after an initial experience with saccharin, albeit a relatively short exposure. The absence of immediate line differences with infusion procedures suggests that preference differences for saccharin between HiS and LoS lines are not mediated by brainstem taste reflexes, but rather are guided by associative processes accomplished above the brainstem.

Taste reactivity in rats selectively bred for high vs. low saccharin consumption.

Rats selectively bred for high (HiS) vs. low (LoS) saccharin consumption were compared on taste reactivity responses to 0.1% saccharin before and after continuous access to 0.1% saccharin. The rats were also tested with other saccharin concentrations (0.01-0.3%) before and after the consumption test. Finally, all rats were tested for reactivity to 0.1 M sucrose, 0.0001 M quinine hydrochloride, and a sucrose + quinine mixture. HiS rats ingested more saccharin than did LoS rats, but the groups did not differ in total ingestive or total aversive reactivity on any of the taste tests. When aversive reactivity was analyzed further to distinguish passive drip from other, more active responses, HiS rats made more active responses than LoS rats; the latter showed a consistent tendency to passive drip more than HiS rats. Overall, aversive responding decreased and ingestive responding increased as saccharin concentration rose and from the first to the second concentration series. Because the brain stem-mediated hedonic evaluation of tastes by HiS and LoS rats appears to be similar, the difference in saccharin consumption must be mediated by psychological processes whose neural substrates lie above the brain stem.

Delayed generalization testing produces enhanced alcohol aversions in rats.

Three experiments examined the effects of the training-to-testing interval on alcohol aversions. In Experiments 1 and 2, rats learned a taste aversion to a 4% (v/v) alcohol solution using lithium chloride as the illness agent. With a between-groups design, subjects were tested with 1%, 4%, or 7% alcohol, beginning either 2 or 21 days after training. In both experiments, results showed that rats learned aversions to the trained 4% alcohol that generalized to the nontrained 1% and 7% concentrations. Furthermore, in Experiment 1 aversions to 1% and 7% alcohol were stronger in groups tested 21 days after training relative to groups tested 2 days after training. When the strength of the illness agent was reduced in Experiment 2, aversions to all concentrations of alcohol were stronger at the delayed testing interval. Experiment 3 ruled out the possibility that enhanced alcohol avoidance at delayed testing was the result of spontaneous recovery of neophobia. The results suggest that taste aversions to alcohol become stronger with time. Possible mechanisms for this "incubation effect" are discussed. The present findings have implications for improving emetic therapy as a treatment for human alcoholics.

Taste reactivity and consumption measures in the assessment of overshadowing: Modulation of aversive, but not ingestive, reactivity.

Three dependent measures-a taste reactivity test, a two-bottle preference test, and a one-bottle extinction test-were used to investigate the conditioning effects of pairing a taste/taste compound with LiCl-induced illness in rats. Avoidance of saccharin consumption in the one-bottle test was attenuated if saccharin and denatonium were paired during illness training (overshadowing). Also, saccharin was found to be more palatable if paired with denatonium during training as reflected by aversive (but not ingestive) taste reactivity measures. It is argued that overshadowing was reflected mainly by a modulation of aversive taste reactivity behavior with little influence on ingestive taste reactivity. The results are discussed in terms of current palatability issues, and it is suggested that applying taste reactivity tests to phenomena associated with taste avoidance learning (e.g., overshadowing or potentiation) may further our understanding of the mechanisms that guide such learning.

Taste reactivity in high alcohol drinking and low alcohol drinking rats.

High alcohol drinking (HAD) and low alcohol drinking (LAD) rats were tested, in three exposures, for taste reactivity to five concentrations of alcohol (5%, 10%, 20%, 30%, and 40%, v/v), water, and one concentration each of sucrose and quinine. Of the three reactivity exposures, one was done before a 3-week period of continuous access to water and 10% alcohol, the second test was done immediately after the consumption period, and the final reactivity test was done after 1 month of alcohol abstinence. The results showed that the groups did not differ in reactivity on the initial test. After the consumption tests (when the HAD rats consumed significantly more alcohol than the LAD rats), differences in reactivity were found: HAD rats produced significantly more ingestive responses (which promote consumption) and significantly fewer aversive responses (which facilitate fluid rejection) than LAD rats. These differences were maintained even after 1 month of alcohol abstinence. The present data replicate an earlier experiment with alcohol-preferring (P) rats and alcohol-non-preferring (NP) rats, and indicate that the selective breeding process does not produce differences in the innate perception of the taste of alcohol. However, after experience with drinking alcohol, rats selectively bred for high alcohol consumption exhibit a palatability shift reflected by high ingestive responding and little or no aversive responding. Such a shift would clearly contribute to the maintenance of high levels of alcohol consumption.

Tryptophan deficiency and alcohol consumption in rats as a model for disadvantaged human populations: a preliminary study.

Choice of diet is a combination of socioeconomic, psychological, and biological factors. This article reports on a preliminary study using an animal model and approximating the dietary conditions found on some Native American reservations. The results suggest that alcohol consumption in these disadvantaged populations may be a result of tryptophan deficiency. Tryptophan-deficient rats consumed more alcohol under ad-libitum conditions, perhaps to compensate for the lack of this essential amino acid. Tryptophan is the biological precursor of serotonin, a central neurotransmitter that has been implicated in mood elevations and declines. Alcohol has been found to mimic the effects of tryptophan or serotonin. We suggest that alcohol consumption may act to compensate for the dietary deficiency of this amino acid. The model attributing alcohol consumption to tryptophan deficiency thus connects socioeconomic, psychological, and biological factors.

Alcohol, palatability, and taste reactivity.

The taste reactivity procedure provides a valuable tool for examining issues of palatability of alcohol solutions for rats. Given that alcohol is normally introduced to the internal milieu orally, taste factors must play an important role in the animal's decision to ingest or reject. Extensive studies of rats' reactivity to alcohol solutions have revealed several important variables that appear to affect palatability: solution concentration, alcohol experience, and postingestive consequences. In a recent selective breeding project, it has been found that taste reactivity to alcohol has a high heritability in rats. High ingestive responding and low ingestive responding rats were selected and bred to produce two lines. In the first selected generation, calculation of the realized heritability was 0.43; the cumulative realized heritability using the data from the second selected generation was 0.68. The introduction of the taste reactivity paradigm to the field of behavioral genetics may provide important information for the study of genetics, chemical senses, and alcohol consumption.

Alterations in taste reactivity to alcohol in rats given continuous alcohol access followed by abstinence.

Naive, male rats (n = 14) were given continuous access to 10% alcohol and water for a period of 6 weeks. Concurrent taste reactivity tests showed a consistent increase in ingestive responding to a range of alcohol concentrations (10%-40%) over the course of alcohol access. The rats also showed a consistent decrease in aversive responding over time. These data suggested that the palatability of alcohol increased with alcohol experience. After a 1-month period of alcohol abstinence, however, ingestive taste reactivity to alcohol returned to the same level as that found when the rats were alcohol naive, whereas aversive responding approached the level seen initially. A separate control group (n = 13) given only water for the same length of time failed to show similar changes in taste reactivity to alcohol solutions.

Gustatory and olfactory contributions to alcohol consumption in rats.

To determine the relative contributions of taste and smell in the consumption of alcohol by rats, the present experiment tested normal rats (n = 14) and rats with either gustatory cortex ablations (n = 10), olfactory bulbectomies (n = 11), or combination gustatory cortex and olfactory bulb ablations (n = 12). Rats were tested under mild fluid deprivation using a two-bottle testing procedure. Thirteen concentrations of alcohol (0.5%, 1%, 2%, 3%, 4%, 5%, 6%, 7%, 8%, 9%, 10%, 11%, and 12%, v/v) were tested in ascending order. Results showed that at strong alcohol concentrations (7% through 11%) rats with combined gustatory cortex and olfactory bulb ablations consumed significantly more alcohol than normal control rats. Rats lacking gustatory cortex displayed a similar increased level of consumption with strong alcohol concentrations. It is suggested that the high level of consumption of strong alcohol concentrations by rats with central nervous system damage reflects an associative deficit rather than an alteration in taste or odor perception.

Evaluating the palatability of alcohol for rats with measures of taste reactivity, consumption, and lick rate.

In two experiments, rats were presented with water and six concentrations of alcohol (0.5%, 3%, 6%, 9%, 12%, and 15%, v/v) under conditions of mild fluid deprivation. Their responses were measured using taste reactivity (fluids infused directly into the mouth), consumption, and lick rate (both in a voluntary drinking situation). Results in both experiments showed that the number of overall ingestive responses was relatively high and consistent across all alcohol concentrations and water; aversive responding was low for all solutions. During one-bottle, 10-min tests, rats consumed the three lowest concentrations of alcohol (0.5%, 3%, and 6%) and water at an equal level. There was an abrupt drop in the amount of alcohol consumed at 9% and a continued decrease at the two highest concentrations. Lick rates for alcohol (measured only in Experiment 2) fell into three general patterns: 0.5%, 3%, and 6% produced almost identical, negatively accelerating curves consistently above that of water which was linear; lick rates for 9% and 12% rose initially but, at approximately 2 min, became flat; the 15% solution produced a low lick rate throughout the 5-min period. There were significant correlations between lick rate and amount consumed but, contrary to expectations, no significant correlations were found between taste reactivity and the other two measures (consumption and lick rate). These results suggest that taste reactivity to alcohol solutions may be reflective of processes different from those that regulate licking behavior or actual consumption.

Taste avoidance, but not aversion, learning in rats lacking gustatory cortex.

Control rats rapidly learned to avoid drinking either a sucrose solution (Experiment 1) or a NaCl solution (Experiment 2) when the taste was paired with illness. These rats also produced aversive reactivity to each of these solutions in a taste reactivity test. Rats that lacked gustatory cortex (GC) learned to avoid drinking sucrose and NaCl, albeit at a slower rate than control rats. GC rats failed to display aversive reactivity to these tastes. The GC rats did show normal aversive reactivity to a strong quinine HCl solution during additional tests. It is suggested that the avoidance developed by GC rats did not entail a palatability shift of the conditional stimulus as it did in control rats. This altered learning strategy may account for the consistent learning deficits found in GC rats trained to avoid tastes.

Odor cue mediation of alcohol aversion learning in rats lacking gustatory neocortex.

Normal rats presented with a 5% alcohol solution followed by lithium chloride-induced illness quickly learned to avoid drinking alcohol. After training, the rats also avoided drinking water in the presence of the alcohol odor alone, whether tested immediately or 1 month later. In Experiment 1, rats with gustatory neocortex (GN) ablations also developed strong alcohol aversions when the alcohol solution was paired with illness. They also showed normal avoidance of drinking in the presence of the alcohol odor alone when tested soon after training. In Experiment 2, when normal rats were trained to avoid alcohol, given GN ablations, and then tested for retention 1 month later, avoidance of drinking water in the presence of the odor alone was significant but attenuated somewhat in relation to trained control rats. These data support the hypothesis that rats lacking GN partially acquire alcohol aversions by using odor cues and confirm that associative learning is intact in these rats despite the fact that GN rats display significant deficits in aversion learning when only tastes are paired with illness.

Taste reactivity in alcohol preferring and nonpreferring rats.

Taste reactivity tests were used to examine the orofacial responses of alcohol preferring (P) rats and alcohol nonpreferring (NP) rats to the taste of alcohol. In the initial exposure, naive rats were tested for reactivity to five concentrations of alcohol (5%, 10%, 20%, 30%, and 40% v/v), water, and one solution each of sucrose and quinine. A two-bottle consumption test was then given for a 3-week period to allow the rats access to 10% alcohol. After the preference test, a second taste reactivity test was done using the same solutions as in the initial reactivity test. The results indicated no significant differences in taste reactivity between P rats and NP rats on the initial exposure, except that NP rats made significantly more mouth movements. During the two-bottle tests, consumption of alcohol by P rats was consistently higher than that of NP rats across all test days. On the second taste reactivity test, P rats showed an increase in the number of ingestive responses and a decrease in the number of aversive responses to alcohol. NP rats' taste reactivity to alcohol remained unchanged from Exposure 1 to Exposure 2. P rats' and NP rats' responses to sucrose and quinine did not change from Exposure 1 to Exposure 2. It was concluded that there were no innate taste response differences between P and NP rats to alcohol but that following alcohol experience, P rats showed a significant increase in ingestive responses and a concomitant decrease in aversive responses to the taste of alcohol.(ABSTRACT TRUNCATED AT 250 WORDS)

Similarity of taste reactivity responses to alcohol and sucrose mixtures in rats.

The orofacial responses of rats following infusion of taste solutions were examined in two experiments. In the first experiment, naive rats were presented with a 6% alcohol solution and three sucrose mixtures (sucrose combined with quinine hydrochloride, hydrochloric acid, and sodium chloride, respectively) on separate trials and the resulting taste reactivity was examined. The only difference among the solutions was that alcohol elicited a significantly larger number of aversive responses (e.g., gapes, passive drips) than the sucrose mixtures. In the second experiment, naive rats were trained to avoid 6% alcohol using standard conditioned aversion procedures; rats were then tested for reactivity to the three sucrose mixtures and the alcohol solution. With the alcohol solution, trained rats displayed significantly fewer ingestive responses and significantly more aversive responses than control rats. The response of trained rats to the sucrose + quinine solution was similar to that of alcohol: fewer ingestive responses and more aversive responses than control rats. The number of aversive responses to the alcohol and the sucrose + quinine mixture by the trained rats did not differ significantly. Reactivity to the sucrose + hydrochloric acid and sucrose + sodium chloride solutions did not differ between trained rats and control rats. The results suggest that a sucrose + quinine solution has a perceived taste (as revealed by elicited orofacial reflexes) similar to alcohol and that the sucrose mixture is avoided by rats with alcohol aversions because it is unpalatable.