Molecular mechanisms of maternal cannabis and cigarette use on human neurodevelopment

被引:80
作者
Morris, Claudia V. [1 ,2 ]
DiNieri, Jennifer A. [1 ,2 ]
Szutorisz, Henrietta [1 ]
Hurd, Yasmin L. [1 ,2 ,3 ]
机构
[1] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA
[2] Mt Sinai Sch Med, Dept Neurosci, New York, NY USA
[3] Mt Sinai Sch Med, Dept Pharmacol & Syst Therapeut, New York, NY USA
基金
美国国家卫生研究院;
关键词
epigenetics; fetal; marijuana; nicotine; prenatal; PRENATAL MARIJUANA EXPOSURE; CELL-ADHESION MOLECULE; PROENKEPHALIN GENE-EXPRESSION; NICOTINE EXPOSURE; BRAIN-REGIONS; PERINATAL EXPOSURE; MESSENGER-RNA; SMOKE EXPOSURE; ACETYLCHOLINE-RECEPTORS; DOPAMINE-RECEPTORS;
D O I
10.1111/j.1460-9568.2011.07884.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:1574 / 1583
页数:10
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