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  1. Article: Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.

    Bottom, Riley T / Kozanian, Olga O / Rohac, David J / Erickson, Michael A / Huffman, Kelly J

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 812429

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2022-03-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.812429
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Long-Lasting Effects of Prenatal Ethanol Exposure on Fear Learning and Development of the Amygdala.

    Kozanian, Olga O / Rohac, David J / Bavadian, Niusha / Corches, Alex / Korzus, Edward / Huffman, Kelly J

    Frontiers in behavioral neuroscience

    2018  Volume 12, Page(s) 200

    Abstract: Prenatal ethanol exposure (PrEE) produces developmental abnormalities in brain and behavior that often persist into adulthood. We have previously reported abnormal cortical gene expression, disorganized neural circuitry along with deficits in ... ...

    Abstract Prenatal ethanol exposure (PrEE) produces developmental abnormalities in brain and behavior that often persist into adulthood. We have previously reported abnormal cortical gene expression, disorganized neural circuitry along with deficits in sensorimotor function and anxiety in our CD-1 murine model of fetal alcohol spectrum disorders, or FASD (El Shawa et al., 2013; Abbott et al., 2016). We have proposed that these phenotypes may underlie learning, memory, and behavioral deficits in humans with FASD. Here, we evaluate the impact of PrEE on fear memory learning, recall and amygdala development at two adult timepoints. PrEE alters learning and memory of aversive stimuli; specifically, PrEE mice, fear conditioned at postnatal day (P) 50, showed deficits in fear acquisition and memory retrieval when tested at P52 and later at P70-P72. Interestingly, this deficit in fear acquisition observed during young adulthood was not present when PrEE mice were conditioned later, at P80. These mice displayed similar levels of fear expression as controls when tested on fear memory recall. To test whether PrEE alters development of brain circuitry associated with fear conditioning and fear memory recall, we histologically examined subdivisions of the amygdala in PrEE and control mice and found long-term effects of PrEE on fear memory circuitry. Thus, results from this study will provide insight on the neurobiological and behavioral effects of PrEE and provide new information on developmental trajectories of brain dysfunction in people prenatally exposed to ethanol.
    Language English
    Publishing date 2018-09-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452960-6
    ISSN 1662-5153
    ISSN 1662-5153
    DOI 10.3389/fnbeh.2018.00200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASD.

    Abbott, Charles W / Rohac, David J / Bottom, Riley T / Patadia, Sahil / Huffman, Kelly J

    Cerebral cortex (New York, N.Y. : 1991)

    2017  Volume 28, Issue 8, Page(s) 2908–2921

    Abstract: Fetal Alcohol Spectrum Disorders, or FASD, represent a range of adverse developmental conditions caused by prenatal ethanol exposure (PrEE) from maternal consumption of alcohol. PrEE induces neurobiological damage in the developing brain leading to ... ...

    Abstract Fetal Alcohol Spectrum Disorders, or FASD, represent a range of adverse developmental conditions caused by prenatal ethanol exposure (PrEE) from maternal consumption of alcohol. PrEE induces neurobiological damage in the developing brain leading to cognitive-perceptual and behavioral deficits in the offspring. Alcohol-mediated alterations to epigenetic function may underlie PrEE-related brain dysfunction, with these changes potentially carried across generations to unexposed offspring. To determine the transgenerational impact of PrEE on neocortical development, we generated a mouse model of FASD and identified numerous stable phenotypes transmitted via the male germline to the unexposed third generation. These include alterations in ectopic intraneocortical connectivity, upregulation of neocortical Rzrβ and Id2 expression accompanied by both promoter hypomethylation of these genes and decreased global DNA methylation levels. DNMT expression was also suppressed in newborn PrEE cortex, providing further insight into how ethanol perturbs DNA methylation leading to altered regulation of gene transcription. These PrEE-induced, transgenerational phenotypes may be responsible for cognitive, sensorimotor, and behavioral deficits seen in humans with FASD. Thus, understanding the possible epigenetic mechanisms by which these phenotypes are generated may reveal novel targets for therapeutic intervention of FASD and lead to advances in human health.
    MeSH term(s) Animals ; Animals, Newborn ; Body Weight/drug effects ; Central Nervous System Depressants/toxicity ; DNA Methylation/drug effects ; Developmental Disabilities/etiology ; Developmental Disabilities/pathology ; Disease Models, Animal ; Epigenomics ; Ethanol/toxicity ; Female ; Fetal Alcohol Spectrum Disorders/etiology ; Fetal Alcohol Spectrum Disorders/pathology ; Fetal Alcohol Spectrum Disorders/physiopathology ; Male ; Mice ; Mood Disorders/etiology ; Motor Activity/physiology ; Neocortex/growth & development ; Neocortex/pathology ; Neurons/pathology ; Pregnancy ; Prenatal Exposure Delayed Effects/physiopathology ; RNA, Messenger/metabolism ; Self Administration
    Chemical Substances Central Nervous System Depressants ; RNA, Messenger ; Ethanol (3K9958V90M)
    Language English
    Publishing date 2017-11-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1077450-6
    ISSN 1460-2199 ; 1047-3211
    ISSN (online) 1460-2199
    ISSN 1047-3211
    DOI 10.1093/cercor/bhx168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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