PubMed Health⌕ Search

Biomedical subjects

Amanda L Sharpe

Publications and source records attributed to Amanda L Sharpe.

3 recordsLinked to original sources

Ethanol and sucrose self-administration components: effects of drinking history.

Results of previous studies have shown that when rats consume higher concentrations of ethanol during initiation both the amount consumed and the pattern of consumption change with the return to a lower concentration. In this study, an across-sessions breakpoint procedure in the sipper-tube model was used to examine the effect that experience with drinking higher concentrations (a concentration manipulation) of both ethanol and sucrose had on appetitive and consummatory behaviors. A follow-up study was then conducted in the ethanol-consuming group with across-session breakpoint and intake examined before, during, and after a 3% sucrose/10% ethanol solution was presented in the sipper tube. As ethanol concentration increased, intake was not changed. Exposure to higher ethanol concentrations had no effect on the amount of 10% ethanol consumed when retested. The exposure tended to increase appetitive behavior (breakpoint), but this effect was not unique to ethanol, as rats self-administering 3% sucrose showed a similar increase. When the combined ethanol-sucrose solution was available, a significant increase in both intake and appetitive responding occurred; however, there was no change from prior intake or breakpoint when 10% ethanol was retested. That the addition of sucrose to the ethanol solution significantly increased appetitive and consummatory behaviors supports the suggestion that the composition of the alcoholic beverage can have a strong influence over the control of self-administration. Because most consumption of ethanol by human beings is in solutions that contain mixers that alter the taste of the solution, this taste factor needs to be considered in the regulation of ethanol drinking.

Alcohol Drinking↗

Repeated nicotine injections decrease operant ethanol self-administration.

Nicotine and alcohol are two of the most used drugs in the United States. However, it is not clear whether the co-use of these drugs is due to pharmacological or environmental reasons, or perhaps related to both. Although results from previous studies in animal models seem to indicate that nicotine has an effect on ethanol consumption, little has been done to determine how nicotine affects appetitive and consummatory phases of ethanol self-administration. In this study, we examined the effect of repeated treatment with nicotine (0, 0.35, and 0.7 mg/kg, s.c.), given 30 min before a daily operant session, on appetitive and consummatory phases of Long-Evans rats self-administering 10% (vol./vol.) ethanol in a sipper-tube model. Ethanol intake (consummatory phase) decreased at both doses of nicotine tested, and lever pressing (appetitive phase) decreased after injection of the high dose of nicotine. These results support the suggestion that nicotine affects ethanol self-administration. However, in this model, the findings demonstrate a reduction in drinking, rather than the enhancement that has been shown in findings obtained from other studies.

Animals↗

Effect of ethanol self-administration on mu- and delta-opioid receptor-mediated G-protein activity.

BACKGROUND: This study examined the effects of ethanol self-administration on mu- and delta-opioid receptor-mediated G-protein activity in specific brain regions of male Long Evans rats. METHODS: Rats were trained to self-administer ethanol by using a home-cage modification of the sucrose substitution paradigm. After 30 to 40 days of sucrose or sucrose/15% ethanol self-administration (20 min sessions, Monday-Friday), rats were killed for autoradiographic assays. Coronal sections of brains from sucrose and ethanol self-administering rats were collected and processed for basal and mu- and delta-stimulated [35S]guanosine-5'-O-(gamma-thio)-triphosphate (GTPgammaS) binding. Sections were exposed to film and then analyzed by using computer-assisted densitometry to determine levels of basal and agonist-stimulated [35S]GTPgammaS binding. RESULTS: Mu-opioid-stimulated [35S]GTPgammaS binding was decreased in the prefrontal cortex of brains from ethanol compared with sucrose self-administering rats. Mu-opioid-stimulated [35S]GTPgammaS binding was unchanged in the cingulate cortex, caudate-putamen, nucleus accumbens, amygdala, hypothalamus, thalamus, and locus ceruleus of ethanol compared with sucrose self-administering rats. Basal and delta-opioid-stimulated [35S]GTPgammaS binding did not differ between the two groups in the prefrontal cortex or any other region analyzed. CONCLUSIONS: These data demonstrate decreased mu-opioid-mediated G-protein activity in the prefrontal cortex of ethanol self-administering rats and suggest an interaction between ethanol and mu-opioid receptors in this region.

Animals↗