Special Issue "Molecular and Cellular Mechanisms Mediating the Behavioral Effects of Alcohol"

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Systems Neuroscience".

Deadline for manuscript submissions: 30 December 2019.

Special Issue Editor

Guest Editor
Dr. Candice Contet Website E-Mail
The Scripps Research Institute, Department of Neuroscience, La Jolla, CA, USA
Interests: alcohol; dependence; self-administration; stress; negative affect; neuropeptides; ion channels; microtubules; parasubthalamic nucleus; mouse models

Special Issue Information

Dear Colleagues,

Alcoholic beverages are commonly consumed for the positively reinforcing properties of their molecular constituent, ethanol. At different doses, ethanol can produce a variety of behavioral effects, ranging from euphoria to anxiolysis, appetite stimulation, cognitive and motor alterations, aggression, sedation, and coma. Pathological patterns of alcohol consumption can alter the initial response to ethanol, and additional behavioral changes emerge during acute withdrawal and protracted abstinence from alcohol (e.g., seizures, craving, negative affect). Alcohol exposure during adolescence, gestation, and gametogenesis can also have a long-term impact on behaviors later in life and across generations, as a result of developmental and epigenetic effects. Identifying the stuctural and functional changes in specific brain regions, cell populations, or neural circuits which causally contribute to the behavioral phenotypes associated with ethanol exposure and withdrawal is essential to our understanding of the neurobiological mechanisms underlying alcohol’s action. It also represents a critical endeavor for the development of rational approaches to leverage the desirable properties of ethanol and to alleviate the burden associated with the detrimental consequences of excessive alcohol consumpion.

Original research articles advancing our understanding of the “Molecular and Cellular Mechanisms Mediating the Behavioral Effects of Ethanol” are solicited for this Special Issue. Reviews providing an analytical perspective on the existing literature are also welcome.

Dr. Candice Contet
Guest Editor

Manuscript Submission Information

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Keywords

  • intoxication
  • binge drinking
  • dependence
  • addiction
  • relapse
  • alcohol use disorders
  • genes
  • proteins
  • signaling pathways
  • medication development

Published Papers (3 papers)

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Research

Open AccessArticle
Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice
Brain Sci. 2019, 9(7), 171; https://doi.org/10.3390/brainsci9070171 - 19 Jul 2019
Abstract
Corticotropin releasing factor (CRF) signaling via limbic CRF1 and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate binge-like ethanol consumption in rodents. Though CRF signaling in the medial prefrontal cortex (mPFC) has been shown to modulate anxiety-like behavior and ethanol seeking, [...] Read more.
Corticotropin releasing factor (CRF) signaling via limbic CRF1 and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate binge-like ethanol consumption in rodents. Though CRF signaling in the medial prefrontal cortex (mPFC) has been shown to modulate anxiety-like behavior and ethanol seeking, its role in binge ethanol intake is unknown. Here, we used “drinking-in-the-dark” (DID) procedures in male and female C57BL/6J mice to address this gap in the literature. First, the role of CRF1R and CRF2R signaling in the mPFC on ethanol consumption was evaluated through site-directed pharmacology. Next, we evaluated if CRF1R antagonist reduction of binge-intake was modulated in part through CRF2R activation by co-administration of a CRF1R and CRF2R antagonist. Intra-mPFC inhibition of CRF1R and activation of CRF2R resulted in decreased binge-like ethanol intake. Further, the inhibitory effect of the CRF1R antagonist was attenuated by co-administration of a CRF2R antagonist. We provide novel evidence that (1) inhibition of CRF1R or activation of CRF2R in the mPFC reduces binge-like ethanol intake; and (2) the effect of CRF1R antagonism may be mediated via enhanced CRF2R activation. These observations provide the first direct behavioral pharmacological evidence that CRF receptor activity in the mPFC modulates binge-like ethanol consumption. Full article
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Open AccessArticle
Sex Differences in the Effect of Alcohol Drinking on Myelinated Axons in the Anterior Cingulate Cortex of Adolescent Rats
Brain Sci. 2019, 9(7), 167; https://doi.org/10.3390/brainsci9070167 - 16 Jul 2019
Abstract
Cognitive deficits associated with teenage drinking may be due to disrupted myelination of prefrontal circuits. To better understand how alcohol affects myelination, male and female Wistar rats (n = 7–9/sex/treatment) underwent two weeks of intermittent operant self-administration of sweetened alcohol or sweetened [...] Read more.
Cognitive deficits associated with teenage drinking may be due to disrupted myelination of prefrontal circuits. To better understand how alcohol affects myelination, male and female Wistar rats (n = 7–9/sex/treatment) underwent two weeks of intermittent operant self-administration of sweetened alcohol or sweetened water early in adolescence (postnatal days 28–42) and we tested for macro- and microstructural changes to myelin. We previously reported data from the males of this study showing that alcohol drinking reduced myelinated fiber density in layers II–V of the anterior cingulate division of the medial prefrontal cortex (Cg1); herein, we show that myelinated fiber density was not significantly altered by alcohol in females. Alcohol drinking patterns were similar in both sexes, but males were in a pre-pubertal state for a larger proportion of the alcohol exposure period, which may have contributed to the differential effects on myelinated fiber density. To gain more insight into how alcohol impacts myelinated axons, brain sections from a subset of these animals (n = 6/sex/treatment) were used for microstructural analyses of the nodes of Ranvier. Confocal analysis of nodal domains, flanked by immunofluorescent-labeled contactin-associated protein (Caspr) clusters, indicated that alcohol drinking reduced nodal length-to-width ratios in layers II/III of the Cg1 in both sexes. Despite sex differences in the underlying cause (larger diameter axons after alcohol in males vs. shorter nodal lengths after alcohol in females), reduced nodal ratios could have important implications for the speed and integrity of neural transmission along these axons in both males and females. Alcohol-induced changes to myelinated axonal populations in the Cg1 may contribute to long-lasting changes in prefrontal function associated with early onset drinking. Full article
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Open AccessArticle
Paternal Preconception Every-Other-Day Ethanol Drinking Alters Behavior and Ethanol Consumption in Offspring
Brain Sci. 2019, 9(3), 56; https://doi.org/10.3390/brainsci9030056 - 06 Mar 2019
Abstract
Alcohol use disorder is a devastating disease with a complex etiology. Recent preclinical studies have revealed that paternal preconception chronic intermittent ethanol (EtOH) exposure via vaporized EtOH altered drinking behaviors and sensitivity to EtOH selectively in male offspring. In the current study, we [...] Read more.
Alcohol use disorder is a devastating disease with a complex etiology. Recent preclinical studies have revealed that paternal preconception chronic intermittent ethanol (EtOH) exposure via vaporized EtOH altered drinking behaviors and sensitivity to EtOH selectively in male offspring. In the current study, we used a voluntary oral route of paternal preconception EtOH exposure, i.e., intermittent every-other-day two-bottle choice drinking, and tested offspring for behavioral alterations. Fifteen EtOH drinking sires and 10 control sires were mated to EtOH naïve females to produce EtOH-sired and control-sired offspring. These offspring were tested using the elevated plus maze, open field, drinking in the dark, and unlimited access two-bottle choice assays. We found that paternal preconception every-other-day two-bottle choice drinking resulted in reduced EtOH consumption selectively in male offspring in the drinking in the dark assay compared to control-sired offspring. No differences were detected in either sex in the unlimited access two-bottle choice and elevated plus maze assays. Open field analysis revealed complex changes in basal behavior and EtOH-induced behaviors that were sex specific. We concluded that paternal preconception voluntary EtOH consumption has persistent effects that impact the next generation. This study adds to a growing appreciation that one’s behavioral response to EtOH and EtOH drinking behavior are impacted by EtOH exposure of the prior generation. Full article
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