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Molecular mechanisms of maternal cannabis and cigarette use on human neurodevelopment

Authors

  • Claudia V. Morris,

    1. Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA
    2. Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA
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  • Jennifer A. DiNieri,

    1. Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA
    2. Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA
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  • Henrietta Szutorisz,

    1. Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA
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  • Yasmin L. Hurd

    1. Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA
    2. Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA
    3. Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY, USA
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Y. L. Hurd, as above.
E-mail: yasmin.hurd@mssm.edu

Abstract

Prenatal development is highly sensitive to maternal drug use due to the vulnerability for disruption of the fetal brain with its ongoing neurodevelopment, resulting in lifelong consequences that can enhance risk for psychiatric disorders. Cannabis and cigarettes are the most commonly used illicit and licit substances, respectively, among pregnant women. Although the behavioral consequences of prenatal cannabis and cigarette exposure have been well-documented in epidemiological and clinical studies, only recently have investigations into the molecular mechanisms associated with the developmental impact of early drug exposure been addressed. This article reviews the literature relevant to long-term gene expression disturbances in the human fetal brain in relation to maternal cannabis and cigarette use. To provide translational insights, we discuss animal models in which protracted molecular consequences of prenatal cannabis and cigarette exposure can be better explored and which enable future evaluation of epigenetic pathways, such as DNA methylation and histone modification, that could potentially maintain abnormal gene regulation and related behavioral disturbances. Altogether, this information may help to address the current gaps of knowledge regarding the impact of early drug exposure that set in motion lifelong molecular disturbances that underlie vulnerability to psychiatric disorders.

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