Serotonergic and Dopaminergic Involvement in Ethanol Intake

1992 ◽  
pp. 68-82 ◽  
Author(s):  
J. A. Engel ◽  
C. Enerback ◽  
C. Fahlke ◽  
P. Hulthe ◽  
E. Hard ◽  
...  
Keyword(s):  
Ethanol Intake

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.

scholarly journals Effects of systemic glycine on accumbal glycine and dopamine levels and ethanol intake in male Wistar rats

2020 ◽  
Author(s):  
Yasmin Olsson ◽  
Helga Höifödt Lidö ◽  
Klara Danielsson ◽  
Mia Ericson ◽  
Bo Söderpalm
Keyword(s):  
Wistar Rats ◽  
In Vivo Microdialysis ◽  
Ethanol Intake ◽  
Water Model ◽  
Glycine Transporter 1 ◽  
Improved Outcomes ◽  
Male Wistar Rats ◽  
Treatment Principle ◽  
Reward Pathway

AbstractApproved medications for alcohol use disorder (AUD) display modest effect sizes. Pharmacotherapy aimed at the mechanism(s) by which ethanol activates the dopamine reward pathway may offer improved outcomes. Basal and ethanol-induced accumbal dopamine release in the rat involve glycine receptors (GlyR) in the nucleus accumbens (nAc). Glycine transporter 1 (GlyT-1) inhibitors, which raise extracellular glycine levels, have repeatedly been shown to decrease ethanol intake in the rat. To further explore the rational for elevating glycine levels in the treatment of AUD, this study examined accumbal extracellular glycine and dopamine levels and voluntary ethanol intake and preference in the rat, after systemic treatment with glycine. The effects of three different doses of glycine i.p. on accumbal glycine and dopamine levels were examined using in vivo microdialysis in Wistar rats. In addition, the effects of the intermediate dose of glycine on voluntary ethanol intake and preference were examined in a limited access two-bottle ethanol/water model in the rat. Systemic glycine treatment increased accumbal glycine levels in a dose-related manner, whereas accumbal dopamine levels were elevated in a subpopulation of animals, defined as dopamine responders. Ethanol intake and preference decreased after systemic glycine treatment. These results give further support to the concept of elevating central glycine levels to reduce ethanol intake and indicate that targeting the glycinergic system may represent a pharmacologic treatment principle for AUD.

Photic Regulation of Circadian Rhythms and Voluntary Ethanol Intake: Role of Melanopsin-expressing Intrinsically Photosensitive Retinal Ganglion Cells

2020 ◽  
pp. 074873042098122
Author(s):  
Matthew C. Hartmann ◽  
Walter D. McCulley ◽  
Samuel T. Johnson ◽  
Corey S. Salisbury ◽  
Nikhil Vaidya ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Circadian System ◽  
Genetically Engineered ◽  
Ethanol Intake ◽  
Constant Darkness ◽  
Retinal Ganglion ◽  
Retinal Photoreceptors ◽  
Genetically Engineered Mouse Model ◽  
Lighting Regimen

“Non-image-forming” (NIF) effects of light are mediated primarily by a subset of intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing the photopigment, melanopsin (OPN4). These NIF functions include circadian entrainment, pupillary reflexes, and photic effects on sleep, mood, and cognition. We recently reported that mice of multiple genotypes exhibit reduced voluntary ethanol intake under both constant darkness (DD) and constant light (LL) relative to standard light-dark (LD) conditions. In the present study, we sought to determine whether these effects are mediated by melanopsin-expressing ipRGCs and their potential relationship to photic effects on the circadian system. To this end, we examined the effects of environmental lighting regimen on both ethanol intake and circadian activity rhythms in a genetically engineered mouse model ( Opn4aDTA/aDTA) in which melanopsin expression is completely blocked while ipRGCs are progressively ablated due to activation of attenuated diphtheria toxin A (aDTA) transgene under the control of the Opn4 promoter. As expected from previous studies, Opn4aDTA/aDTA mice displayed dramatic attenuation of circadian photosensitivity, but surprisingly, showed identical suppression of ethanol intake under both DD and LL as that seen in controls. These results demonstrate that the effects of lighting regimen on voluntary ethanol intake are independent of melanopsin-expressing ipRGCs and ipRGC-mediated photic effects on the circadian system. Rather, these effects are likely mediated by classical retinal photoreceptors and central pathways.

A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury

2014 ◽  
Vol 28 (6) ◽  
pp. 739-745 ◽  
Author(s):  
Weichuan Wu ◽  
Runfa Tian ◽  
Shuyu Hao ◽  
Feifan Xu ◽  
Xiang Mao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Ethanol Intake ◽  
High Ethanol

The offspring of alcohol-exposed sires exhibit heightened ethanol intake and behavioral alterations in the elevated plus maze

Alcohol ◽  
2021 ◽  
Vol 92 ◽  
pp. 65-72
Author(s):  
Jennifer Koabel ◽  
Meghan McNivens ◽  
Paul McKee ◽  
Ricardo Pautassi ◽  
Kelly Bordner ◽  
...  
Keyword(s):  
Elevated Plus Maze ◽  
Ethanol Intake ◽  
Behavioral Alterations ◽  
Plus Maze
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