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

基本信息

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
项目类别：
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

项目摘要

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、语言和广义智力的缺陷有关。在子宫内和生命早期接触环境烟草烟雾 (ETS) 也与儿童和青少年时期的神经认知缺陷、行为障碍和智商较低有关。人类大脑在子宫内和生命的第一年经历大量的生长、分化和成熟，使其特别容易受到神经毒性损伤。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，该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 可能对神经化学物质、神经回路和行为发展产生长期影响。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导致早期大脑发育过程中尼古丁暴露的增加。很少有研究对这些多种来源的婴儿尼古丁水平进行量化，而研究尼古丁与早期大脑和神经认知功能之间关系的研究则更少。方法：我们建议在有或没有围产期尼古丁暴露的小婴儿中使用听觉事件相关电位（ERP）来研究可能预示未来神经认知缺陷的神经畸变的生物标志物。我们将检查 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 名不吸烟母亲与吸烟者生活在一起的婴儿 (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、呼出气体以及婴儿尿液中尼古丁暴露的生物标志物。我们将使用经过充分验证的工具来估计适合年龄的发展，重点关注依赖于听觉处理的项目。长期目标是识别和完善尼古丁对发育中大脑有害影响的神经表型，以便为这一重要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。