scholarly journals Absolute ethanol intake predicts ethanol preference in Drosophilamelanogaster

2020 ◽  
Vol 223 (11) ◽  
pp. jeb224121
Author(s):  
Scarlet J. Park ◽  
William W. Ja
Keyword(s):  
Ethanol Intake ◽  
Absolute Ethanol ◽  
Ethanol Preference

scholarly journals CONSTANT ABSOLUTE ETHANOL INTAKE BY SARDINIAN ALCOHOL-PREFERRING RATS INDEPENDENT OF ETHANOL CONCENTRATIONS

1997 ◽  
Vol 32 (1) ◽  
pp. 19-22 ◽  
Author(s):  
C. LOBINA ◽  
R. AGABIO ◽  
G. DIAZ ◽  
M. FA ◽  
F. FADDA ◽  
...  
Keyword(s):  
Ethanol Intake ◽  
Absolute Ethanol

Increased ethanol consumption and blood ethanol levels in rats with portacaval shunts

1985 ◽  
Vol 248 (3) ◽  
pp. G287-G292
Author(s):  
J. R. Martin ◽  
H. Porchet ◽  
R. Buhler ◽  
J. Bircher
Keyword(s):  
Elimination Rate ◽  
Ethanol Intake ◽  
Male Rats ◽  
Chow Diet ◽  
Ethanol Preference ◽  
Low Protein ◽  
Alcohol Dehydrogenase Activity ◽  
Series Of Experiments ◽  
Ad Libitum ◽  
Ethanol Elimination

In a series of experiments, it was demonstrated that male rats with end-to-side portacaval shunts (PCS) consumed more ethanol and exhibited higher blood ethanol levels than sham-operated control animals in chronic tests with 2% ethanol and water ad libitum. Ethanol intake in the 6 h prior to blood sampling was 2-5 times and blood ethanol 10-50 times higher in PCS than control rats. These effects were not due to the feminization of male rats occurring after a PCS, since female PCS rats exhibited comparable increases of ethanol intake and blood ethanol. In both sexes ethanol elimination rate and alcohol dehydrogenase activity per total liver were lower after PCS than in control rats, explaining the disproportionate increase in blood ethanol relative to ethanol intake. Interestingly, ethanol intake was not abnormal in PCS rats fed a low-protein, low-tryptophan diet (corn) alone or as a supplement to the usual chow diet. Such dietary modulation of ethanol preference in this animal model of chronic liver dysfunction merits further attention.

scholarly journals Social Housing Leads to Increased Ethanol Intake in Male Mice Housed in Environmentally Enriched Cages

2021 ◽  
Vol 15 ◽  
Author(s):  
Hannah D. Fulenwider ◽  
Meridith T. Robins ◽  
Maya A. Caruso ◽  
Andrey E. Ryabinin
Keyword(s):  
Social Context ◽  
Social Housing ◽  
Environmental Enrichment ◽  
Alcohol Intake ◽  
Choice Model ◽  
Ethanol Intake ◽  
Nucleus Accumbens Shell ◽  
Group Setting ◽  
Ethanol Preference ◽  
Complex Interactions

An individual's social environment affects alcohol intake. However, the complex interactions between social context and alcohol intake remain understudied in preclinical models. In the present study, we sought to characterize the effects of social housing on voluntary ethanol intake in male C567BL/6J mice using a continuous access two-bottle choice model. This was accomplished using HM2 cages, which allow for the continuous monitoring of individuals' fluid intake through radiofrequency tracking while they remain undisturbed in a group setting. These cages are moderately environmentally enriched compared to standard shoebox cages. By analyzing the levels of voluntary ethanol intake between socially- and individually-housed mice in HM2 cages, we were able to parse apart the effects of environmental enrichment vs. social enrichment. We found that while intake levels were overall lower than those observed when animals are singly housed in standard shoebox cages, socially-housed males consumed significantly more ethanol compared to individually-housed mice, suggesting that while environmental enrichment attenuates ethanol intake, social enrichment may, in fact, potentiate it. This effect was not specific for alcohol, however, in that ethanol preference did not differ as a product of social context. We also found that the total number of non-consummatory channel entries were consistently higher in individually-housed mice. Additionally, a single corticotropin releasing factor receptor 1 antagonist treatment significantly decreased both water and ethanol intake in socially- and individually-housed mice up to 3 h post-treatment, though the effect on water intake was longer lasting. This treatment also significantly decreased the number of non-consummatory channel entries in individually-housed mice, but not in socially-housed mice, suggesting that increased channel visits may be a stress-related behavior. Lastly, we examined blood ethanol concentrations and FosB immunoreactivity to characterize the physiological responses to ethanol intake in socially- and individually-housed mice. The number of FosB-positive cells in the centrally-projecting Edinger-Westphal nucleus and nucleus accumbens shell positively correlated with average baseline ethanol intake in individually-housed mice, but not in socially-housed mice. Overall, we found that social, but not environmental, enrichment can increase ethanol intake in male C57BL/6J mice. Future studies need to test this phenomenon in female mice and assess the generalizability of this finding.

Dopamine agonist modeling of schizophrenia increases ethanol intake in rats

2012 ◽  
Author(s):  
A. Y. Egorov ◽  
E. O. Kutcher ◽  
N. A. Chernikova ◽  
E. V. Filatova
Keyword(s):  
Dopamine Agonist ◽  
Ethanol Intake

Failure of Stress of Electric Shock to Increase Ethanol Intake in Rats

1967 ◽  
Vol 28 (1) ◽  
pp. 132-137 ◽  
Author(s):  
Robert D. Myers ◽  
R. Bruce Holman
Keyword(s):  
Electric Shock ◽  
Ethanol Intake

Activation of Melanocortin-4 Receptor by a Synthetic Agonist Inhibits Ethanolinduced Neuroinflammation in Rats

2020 ◽  
Vol 25 (45) ◽  
pp. 4799-4805 ◽  
Author(s):  
Osvaldo Flores-Bastías ◽  
Gonzalo I. Gómez ◽  
Juan A. Orellana ◽  
Eduardo Karahanian
Keyword(s):  
Prefrontal Cortex ◽  
Alcohol Consumption ◽  
Ethanol Intake ◽  
Neuroinflammatory Response ◽  
Agonist Peptide ◽  
Melanocortin 4 Receptor ◽  
Tnf Α ◽  
Cord Injury ◽  
High Ethanol ◽  
The Brain

Background: High ethanol intake induces a neuroinflammatory response resulting in the subsequent maintenance of chronic alcohol consumption. The melanocortin system plays a pivotal role in the modulation of alcohol consumption. Interestingly, it has been shown that the activation of melanocortin-4 receptor (MC4R) in the brain decreases the neuroinflammatory response in models of brain damage other than alcohol consumption, such as LPS-induced neuroinflammation, cerebral ischemia, glutamate excitotoxicity, and spinal cord injury. Objectives: In this work, we aimed to study whether MC4R activation by a synthetic MC4R-agonist peptide prevents ethanol-induced neuroinflammation, and if alcohol consumption produces changes in MC4R expression in the hippocampus and hypothalamus. Methods: Ethanol-preferring Sprague Dawley rats were selected offering access to 20% ethanol on alternate days for 4 weeks (intermittent access protocol). After this time, animals were i.p. administered an MC4R agonist peptide in the last 2 days of the protocol. Then, the expression of the proinflammatory cytokines interleukin 6 (IL-6), interleukin 1-beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) were measured in the hippocampus, hypothalamus and prefrontal cortex. It was also evaluated if ethanol intake produces alterations in the expression of MC4R in the hippocampus and the hypothalamus. Results: Alcohol consumption increased the expression of MC4R in the hippocampus and the hypothalamus. The administration of the MC4R agonist reduced IL-6, IL-1β and TNF-α levels in hippocampus, hypothalamus and prefrontal cortex, to those observed in control rats that did not drink alcohol. Conclusion: High ethanol consumption produces an increase in the expression of MC4R in the hippocampus and hypothalamus. The administration of a synthetic MC4R-agonist peptide prevents neuroinflammation induced by alcohol consumption in the hippocampus, hypothalamus, and prefrontal cortex. These results could explain the effect of α-MSH and other synthetic MC4R agonists in decreasing alcohol intake through the reduction of the ethanol-induced inflammatory response in the brain.

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