Biomedical subjects

S W Kiefer

Publications and source records attributed to S W Kiefer.

At least 19 recordsLinked to original sources

PubMed2000

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.

Alcohol Drinking↗

PubMed1998

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).

Animals↗

PubMed1998

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.

Alcohol Drinking↗

PubMed1997

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.

Animals↗

PubMed1997

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.

Alcohol Drinking↗

PubMed1995

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.

Animals↗

PubMed1995

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.

Alcoholism↗

PubMed1995

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.

Alcohol Drinking↗

PubMed1994

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.

Alcohol Drinking↗

PubMed1992

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.

Animals↗

PubMed1991

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.

Alcohol Drinking↗

PubMed1990

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)

Alcohol Drinking↗

PubMed1989

Taste reactivity to alcohol in rats.

Rats were infused intraorally with 4 concentrations of ethanol (3%, 6%, 9%, and 12%), and their subsequent oral, facial, and bodily responses were videotaped and analyzed. Naive rats did not display significant changes in ingestive-type responding over the concentrations tested. A significant increase in aversive responses was noted, with the largest number of aversive responses found with the 12% solution. Initial reactivity failed to predict subsequent consumption when rats were given free access to the same alcohol concentrations during 2-bottle tests. Reactivity testing after the period of alcohol access indicated that only the aversive responding changed significantly from the initial reactivity, with rats showing fewer aversive responses. The results indicated how the taste of alcohol is perceived by naive rats and how this perception is changed after consummatory experience with alcohol.

Alcohol Drinking↗

PubMed1988

Alcohol aversion generalization in rats: specific disruption of taste and odor cues with gustatory neocortex or olfactory bulb ablations.

Rats with ablations of the gustatory neocortex (Experiment 1) and rats with olfactory bulb ablations (Experiment 2) were compared with normal rats for aversion generalization to both single taste solutions (sucrose, sodium chloride, quinine hydrochloride, hydrochloric acid) and compound taste solutions (pairs of the four single tastants) following alcohol aversion training. All rats acquired equal and strong alcohol aversions. Control rats showed consistent aversion generalization to both the sucrose + quinine and the sucrose + hydrochloric acid solutions; no significant generalization occurred to the single tastants except a weak generalization to sucrose in Experiment 2. Rats with gustatory neocortical ablations failed to show aversion generalization to any of the taste solutions. Rats with olfactory bulbectomies displayed the same aversion generalization functions as control rats but exhibited significantly faster extinction of the alcohol aversion than did the trained control rats. Results from the present experiments suggest that during alcohol aversion learning, rats lacking gustatory neocortex use odor cues (no taste generalization), whereas rats lacking olfactory bulbs utilize taste cues (normal taste generalization).

Afferent Pathways↗

PubMed1987

Cessation of male rat copulatory behavior using illness as punishment: facilitation with a novel odor.

Two experiments were conducted to examine learned copulatory avoidance in male rats. One group of males was presented with receptive females that had been sprayed with a 2% almond solution, and the other group was presented with nonalmond odorous, receptive females. Following each test, males were made ill with lithium chloride (LiCl) by intragastric intubation or intraperitoneal injection. Results showed that male rats presented with almond-odorous females developed significant avoidance of copulatory behavior. Conditioning in males exposed to receptive females without the almond odor developed little, if any, avoidance. In Experiment 2, it was found that route of LiCl administration was not a factor in the results.

Animals↗

PubMed1986

Flavor-illness aversions: the role of the amygdala in the acquisition of taste-potentiated odor aversions.

In the present experiments the role of the amygdaloid complex and its specific nuclei were tested in the conditioning of taste potentiated odor aversions. In the first experiment two groups of rats were given either large electrolytic lesions in the amygdala (AMX) or sham operations (SH). Postoperatively, these rats were trained to avoid either a taste, an odor, or a taste-odor compound using LiCl illness. Subsequent tests with odor and taste alone showed that the SH group developed strong taste and odor aversions; however, the AMX group failed to display either an odor or taste aversion. In the second experiment, another four groups of rats received either lesions in the medial and basomedial nuclei (M), central nuclei (C), lateral and basolateral (L), or sham operations (SH). The results from postoperative conditioning showed that all groups had strong taste and odor aversions, except group L which displayed a significant disruption of odor aversion learning. In conclusion, these data indicate that the amygdala is involved in the acquisition of taste, odor and potentiated odor aversions learning. Moreover, it is demonstrated that the lateral and/or basolateral nuclei are particularly involved in the development of potentiated odor aversions learning.

Amygdala↗

PubMed1985

Ingestive responses to homeostatic challenges in rats with ablations of the anterolateral neocortex.

Because rats with either anterolateral neocortical or lateral hypothalamic (LH) damage initially display similar feeding and drinking deficits and recovery patterns, the possibility that anterolateral neocortical ablations would also produce similar chronic ingestive impairments to glucoprivic and hydrational challenges was examined. In general, rats with anterolateral neocortical ablations exhibited normal feeding responses to food deprivation and glucoprivation induced by insulin or moderate doses of 2-deoxy-D-glucose (2-DG), but their response to a high dose (500 mg/kg) of 2-DG was impaired. These animals also drank normally in response to hypertonic saline injections and following water deprivation, but only if food was available during the test session, results indicating that they drank prandially. Results indicate that although the anterolateral neocortex and LH are anatomically related, these brain regions appear to be functionally dissimilar in terms of the regulation of ingestion.

Animals↗

PubMed1985

Neural mediation of conditioned food aversions.

The above discussion is only a brief review of what is known about the neural mediation of conditioned food aversions. Although several other approaches were not mentioned (e.g. biochemical studies), one can still appreciate the value of the aversion paradigm for providing important information about neural mechanisms in learning and memory. A theoretical approach that may be valuable in understanding brain function in conditioned food aversion data is Hughlings Jackson's hierarchical notions of nervous organization. Hedonic responses to food stimuli appear to be brainstem reflexes. On top of these are rostral brain structures that add greater complexity to the consummatory behavior of the organism. An important aspect of this complexity is reflected in an animal's ability to form conditioned food aversions, a process undoubtedly tied intimately to particular neural mechanisms.

Afferent Pathways↗