New Advances in Neurobiology and Behavioral Disturbance in Alcohol Use Disorder (AUD) including Fetal Alcohol Spectrum Disorder (FASD)

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

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 7056

Special Issue Editor


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Guest Editor
1. Department of Psychiatry, New York University Langone Medical Center, New York, NY, USA
2. Faculty at Columbia University Medical Center, Scientist, Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, NY, USA
Interests: endocannabinoids; synaptic plasticity; FASD; AUD; neurodegeneration; learning and memory; epigenetics; gene expression; behavior
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Special Issue Information

Dear Colleagues,

Individuals with alcohol use disorders (AUD) suffer from a wide range of interconnected cognitive and psychological problems. However, limited therapeutic possibilities are available for those individuals due to limited investigation of its underlying etiology. In addition, the severity of AUD is influenced by the level and duration of alcohol exposure, developmental stage, genetics, and gender. Interestingly, several recent studies have discovered the essential function of different receptors, neurotransmitters, growth factors, signaling, and epigenetic and genetic influence on gene expression changes that have a distinct role in alcohol abuse-related neurobehavioral impairments.  

This Special Issue of Brain Sciences aims to present a collection of studies focussing on the most recent advancement in alcohol use-related disorders, including fetal alcohol-associated research. Authors are invited to submit cutting-edge reviews, original research articles, and meta-analyses of large existing datasets which advance the field towards a greater understanding of the etiology and pathogenic mechanism. The topics include, without limitation to, studies in epidemiology, neuropsychology, neurobehavior, neuropharmacology, epigenetics, genetics and genomics, brain imaging, molecular neurobiology, experimental model, and clinical investigation. The main format of the publication should be a full-length review or original article. However, other formats with reduced length could also be considered, such as brief reports, short note, communication, or commentary, as long as the manuscript presents innovative and perceptive content that suits the topic of this Special Issue.

Dr. Basavaraj S. Balapal
Guest Editor

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Keywords

  • FASD
  • learning and memory
  • synaptic plasticity
  • alcohol
  • AUD
  • epigenetics
  • genetics

Published Papers (3 papers)

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Research

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23 pages, 3200 KiB  
Article
Effects of Genetics and Sex on Acute Gene Expression Changes in the Hippocampus Following Neonatal Ethanol Exposure in BXD Recombinant Inbred Mouse Strains
by Jessica A. Baker, Jacob T. Brettin, Megan K. Mulligan and Kristin M. Hamre
Brain Sci. 2022, 12(12), 1634; https://doi.org/10.3390/brainsci12121634 - 29 Nov 2022
Cited by 2 | Viewed by 1574
Abstract
Fetal alcohol spectrum disorders (FASD) are prevalent neurodevelopmental disorders. Genetics have been shown to have a role in the severity of alcohol’s teratogenic effects on the developing brain. We previously identified recombinant inbred BXD mouse strains that show high (HCD) or low cell [...] Read more.
Fetal alcohol spectrum disorders (FASD) are prevalent neurodevelopmental disorders. Genetics have been shown to have a role in the severity of alcohol’s teratogenic effects on the developing brain. We previously identified recombinant inbred BXD mouse strains that show high (HCD) or low cell death (LCD) in the hippocampus following ethanol exposure. The present study aimed to identify gene networks that influence this susceptibility. On postnatal day 7 (3rd-trimester-equivalent), male and female neonates were treated with ethanol (5.0 g/kg) or saline, and hippocampi were collected 7hrs later. Using the Affymetrix microarray platform, ethanol-induced gene expression changes were identified in all strains with divergent expression sets found between sexes. Genes, such as Bcl2l11, Jun, and Tgfb3, showed significant strain-by-treatment interactions and were involved in many apoptosis pathways. Comparison of HCD versus LCD showed twice as many ethanol-induced genes changes in the HCD. Interestingly, these changes were regulated in the same direction suggesting (1) more perturbed effects in HCD compared to LCD and (2) limited gene expression changes that confer resistance to ethanol-induced cell death in LCD. These results demonstrate that genetic background and sex are important factors that affect differential cell death pathways after alcohol exposure during development that could have long-term consequences. Full article
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22 pages, 1962 KiB  
Article
Binge-like Prenatal Ethanol Exposure Causes Impaired Cellular Differentiation in the Embryonic Forebrain and Synaptic and Behavioral Defects in Adult Mice
by Shivakumar Subbanna and Balapal S. Basavarajappa
Brain Sci. 2022, 12(6), 793; https://doi.org/10.3390/brainsci12060793 - 17 Jun 2022
Cited by 7 | Viewed by 2532
Abstract
An embryo’s in-utero exposure to ethanol due to a mother’s alcohol drinking results in a range of deficits in the child that are collectively termed fetal alcohol spectrum disorders (FASDs). Prenatal ethanol exposure is one of the leading causes of preventable intellectual disability. [...] Read more.
An embryo’s in-utero exposure to ethanol due to a mother’s alcohol drinking results in a range of deficits in the child that are collectively termed fetal alcohol spectrum disorders (FASDs). Prenatal ethanol exposure is one of the leading causes of preventable intellectual disability. Its neurobehavioral underpinnings warrant systematic research. We investigated the immediate effects on embryos of acute prenatal ethanol exposure during gestational days (GDs) and the influence of such exposure on persistent neurobehavioral deficits in adult offspring. We administered pregnant C57BL/6J mice with ethanol (1.75 g/kg) (GDE) or saline (GDS) intraperitoneally (i.p.) at 0 h and again at 2 h intervals on GD 8 and GD 12. Subsequently, we assessed apoptosis, differentiation, and signaling events in embryo forebrains (E13.5; GD13.5). Long-lasting effects of GDE were evaluated via a behavioral test battery. We also determined the long-term potentiation and synaptic plasticity-related protein expression in adult hippocampal tissue. GDE caused apoptosis, inhibited differentiation, and reduced pERK and pCREB signaling and the expression of transcription factors Pax6 and Lhx2. GDE caused persistent spatial and social investigation memory deficits compared with saline controls, regardless of sex. Interestingly, GDE adult mice exhibited enhanced repetitive and anxiety-like behavior, irrespective of sex. GDE reduced synaptic plasticity-related protein expression and caused hippocampal synaptic plasticity (LTP and LTD) deficits in adult offspring. These findings demonstrate that binge-like ethanol exposure at the GD8 and GD12 developmental stages causes defects in pERK–pCREB signaling and reduces the expression of Pax6 and Lhx2, leading to impaired cellular differentiation during the embryonic stage. In the adult stage, binge-like ethanol exposure caused persistent synaptic and behavioral abnormalities in adult mice. Furthermore, the findings suggest that combining ethanol exposure at two sensitive stages (GD8 and GD12) causes deficits in synaptic plasticity-associated proteins (Arc, Egr1, Fgf1, GluR1, and GluN1), leading to persistent FASD-like neurobehavioral deficits in mice. Full article
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Review

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16 pages, 1000 KiB  
Review
Mechanisms Underlying Cognitive Impairment Induced by Prenatal Alcohol Exposure
by Ahmad Alhowail
Brain Sci. 2022, 12(12), 1667; https://doi.org/10.3390/brainsci12121667 - 04 Dec 2022
Cited by 2 | Viewed by 2446
Abstract
Alcohol is one of the most commonly used illicit substances among pregnant women. Clinical and experimental studies have revealed that prenatal alcohol exposure affects fetal brain development and ultimately results in the persistent impairment of the offspring’s cognitive functions. Despite this, the rate [...] Read more.
Alcohol is one of the most commonly used illicit substances among pregnant women. Clinical and experimental studies have revealed that prenatal alcohol exposure affects fetal brain development and ultimately results in the persistent impairment of the offspring’s cognitive functions. Despite this, the rate of alcohol use among pregnant women has been progressively increasing. Various aspects of human and animal behavior, including learning and memory, are dependent on complex interactions between multiple mechanisms, such as receptor function, mitochondrial function, and protein kinase activation, which are especially vulnerable to alterations during the developmental period. Thus, the exploration of the mechanisms that are altered in response to prenatal alcohol exposure is necessary to develop an understanding of how homeostatic imbalance and various long-term neurobehavioral impairments manifest following alcohol abuse during pregnancy. There is evidence that prenatal alcohol exposure results in vast alterations in mechanisms such as long-term potentiation, mitochondrial function, and protein kinase activation in the brain of offspring. However, to the best of our knowledge, there are very few recent reviews that focus on the cognitive effects of prenatal alcohol exposure and the associated mechanisms. Therefore, in this review, we aim to provide a comprehensive summary of the recently reported alterations to various mechanisms following alcohol exposure during pregnancy, and to draw potential associations with behavioral changes in affected offspring. Full article
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