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(申请人提供)：由母亲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、语言和一般智力的缺陷有关。在宫内和生命早期暴露于环境烟草烟雾(ETS)也与神经认知缺陷、行为障碍以及在儿童和青少年时期测量的低智商有关。人类的大脑在子宫和生命的第一年经历了大量的生长、分化和成熟，这使得它特别容易受到神经毒性的侮辱。尼古丁是一种公认的神经致畸物质，它通过胎盘和血脑屏障与烟碱型乙酰胆碱受体结合，后者广泛参与胎儿和婴儿神经回路的生长、连接和功能发育。因此，PNE或ETS可能会对神经化学、神经回路和行为发育产生长期影响。吸烟母亲的母乳或与吸烟者一起生活的不吸烟母亲的母乳中的尼古丁暴露也可能在大脑发育早期增加尼古丁暴露。从这些多个来源对婴儿尼古丁水平进行量化的研究很少，研究尼古丁与早期大脑和神经认知功能相关的更少。方法：我们建议在有和没有围产期尼古丁暴露的年轻婴儿中使用听觉事件相关电位(ERP)，以研究可能预示未来神经认知缺陷的神经异常的生物标志物。我们将检测3组婴儿的感觉和高阶听觉认知过程：50名吸烟母亲的婴儿(PNE)，50名不吸烟母亲与吸烟者一起生活的婴儿(ETS)，以及50名来自无烟家庭(CTL)的婴儿。我们将测量母亲头发、尿液、呼出的空气和婴儿尿液中尼古丁暴露的生物标记物。我们将使用经过充分验证的工具来估计适合年龄的发育，重点放在依赖于听觉处理的项目上。一个长期目标是识别和提炼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提供早期干预信息。我们计划使用已获得的发现来支持更详细的纵向研究的申请。

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