Perinatal Nicotine and Auditory Evoked Potentials in Early Infancy

围产期尼古丁和婴儿早期听觉诱发电位

• 批准号: 8437138
• 负责人: Karen M Grewen
• 金额: $ 17.76万
• 依托单位: UNIV OF NORTH CAROLINA CHAPEL HILL
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-03-15 至 2015-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8437138
• 关键词: Achievement; Adolescence; Age; Age-Months; Air; Asthma; Attention; Attention Deficit Disorder; Auditory; Auditory Evoked Potentials; Behavior; Behavior Disorders; Behavioral; Binding; Biological Markers; Birth; Blood - brain barrier anatomy; Brain; Breast Feeding; Carbon Monoxide; Child; Childhood; Cigarette; Cognitive; Communication; Control Groups; Cotinine; Data; Defect; Detection; Development; Developmental Process; Differentiation and Growth; Disease; Early Intervention; Electroencephalography; Environment; Environmental Tobacco Smoke; Event-Related Potentials; Exposure to; Future; Goals; Growth; Hair; Health; Health Benefit; Home environment; Human; Human Milk; Impulsivity; Infant; Intelligence; Language; Life; Link; Longitudinal Studies; Low Birth Weight Infant; Measures; Medical Records; Memory; Methods; Mothers; Neurocognitive; Neurocognitive Deficit; Nicotine; Nicotinic Receptors; Outcome; Parents; Performance; Perinatal; Populations at Risk; Postpartum Period; Pregnancy; Pregnant Women; Process; Productivity; Psychotropic Drugs; Public Health; Quality of life; Risk; Risk Factors; Sampling; Sensory; Sensory Process; Short-Term Memory; Sleep; Smoke; Smoker; Smoking; Source; Substance abuse problem; Sudden infant death syndrome; Surveys; TNFRSF5 gene; Techniques; Teratogens; Testing; Third Pregnancy Trimester; Time; Toddler; United States; Urine; Visit; Visual; Visuospatial; activity marker; adverse outcome; brain behavior; cost; critical period; early childhood; fetal; fetal tobacco exposure; in utero; infancy; instrument; maternal cigarette smoking; myelination; neural circuit; neurochemistry; neurotoxic; non-smoking; postnatal; prenatal; prenatal exposure; relating to nervous system; response; sensory gating; skills; tool; urinary

DESCRIPTION (provided by applicant): Prenatal nicotine exposure (PNE) caused by maternal cigarette-smoking is linked to defects in auditory and visual sensory processing, behavior, memory, language, and generalized intelligence. Exposure to environmental tobacco smoke (ETS), in utero and early life is also related to neurocognitive deficits, behavioral disorders, and lower IQ measured in childhood and adolescence. The human brain undergoes massive growth, differentiation and maturation in utero and the first year of life, making it especially vulnerable to neurotoxic insult. Nicotine, a well-documented neural teratogen, crosses the placental and blood brain barriers to bind to nicotinic acetylcholine receptors, which are extensively involved in growth, connectivity and function of developing fetal and infant neural circuits. Thus PNE or ETS may have long term impact on neurochemical, neural circuitry, and behavioral development. Nicotine exposure from breast milk of smoking mothers or from breast milk of non-smoking mothers living with a smoker, may also contribute added nicotine exposure during early brain development. Quantification of infant nicotine levels from these multiple sources has been done in few studies, and fewer still have studied nicotine in association with very early brain and neurocognitive function. Methods: We propose to use auditory event-related potentials (ERP) in young infants with and without perinatal nicotine exposure, to study biological markers of neural aberration that may herald future neurocognitive deficits. We will examine sensory and higher order auditory cognitive processing in 3 groups of infants: 50 infants of mothers who smoke (PNE), 50 infants of non-smoking mothers living with a smoker (ETS), and 50 infants from smoke-free homes (CTL). We will measure biomarkers of nicotine exposure in maternal hair, urine and expired air, and in infant urine. We will use well- validated tools to estimate age-appropriate development focusing on items dependent upon auditory processing. A long term goal is to identify and refine a neurophenotype of nicotine's detrimental effects on the developing brain, in order to inform early interventions in this important at-risk population. We plan to use acquired findings to support an application for more detailed, longitudinal study.

描述（由申请人提供）：母体吸烟引起的产前尼古丁暴露（PNE）与听觉和视觉感觉处理、行为、记忆、语言和广义智力缺陷有关。暴露于环境烟草烟雾（ETS），在子宫内和生命早期也与神经认知缺陷，行为障碍和儿童和青少年时期测量的较低智商有关。人类大脑在子宫内和生命的第一年经历大规模的生长，分化和成熟，使其特别容易受到神经毒性的伤害。尼古丁是一种有据可查的神经致畸剂，可穿过胎盘和血脑屏障与烟碱乙酰胆碱受体结合，烟碱乙酰胆碱受体广泛参与发育中的胎儿和婴儿神经回路的生长、连接和功能。因此，PNE或ETS可能对神经化学，神经回路和行为发育产生长期影响。吸烟母亲或与吸烟者一起生活的非吸烟母亲的母乳中的尼古丁暴露也可能导致早期大脑发育期间的尼古丁暴露增加。在少数几项研究中，对这些多种来源的婴儿尼古丁水平进行了定量分析，研究尼古丁与极早期大脑和神经认知功能相关性的研究更少。研究方法：我们建议使用听觉事件相关电位（ERP）在年轻的婴儿与围产期尼古丁暴露，研究生物标志物的神经畸变，可能预示着未来的神经认知缺陷。我们将研究3组婴儿的感觉和高阶听觉认知处理：50名吸烟母亲的婴儿（PNE），50名与吸烟者生活在一起的非吸烟母亲的婴儿（ETS），以及50名来自无烟家庭的婴儿（CTL）。我们将测量母亲头发、尿液和呼出气体以及婴儿尿液中尼古丁暴露的生物标志物。我们将使用经过验证的工具来估计与年龄相适应的发展，重点是依赖于听觉处理的项目。长期目标是确定和完善尼古丁对发育中大脑的有害影响的神经表型，以便为这一重要的高危人群的早期干预提供信息。我们计划使用获得的发现来支持更详细的纵向研究的应用。

项目成果

Prenatal Nicotine Exposure Disrupts Infant Neural Markers of Orienting.

产前接触尼古丁会扰乱婴儿定向神经标记。

• DOI: 10.1093/ntr/ntx177
• 发表时间: 2018
• 期刊: Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
• 作者: King,Erin;Campbell,Alana;Belger,Aysenil;Grewen,Karen
• 通讯作者: Grewen,Karen