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Alcohol exposure, social behavior and development

酒精暴露、社会行为和发展

基本信息

批准号：
7535041
负责人：
Sandra J Kelly
金额：
$ 38.85万
依托单位：
UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
依托单位国家：
美国
项目类别：
财政年份：
1998
资助国家：
美国
起止时间：
1998-04-08 至 2010-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7535041
关键词：
Address Adolescent Adult Agonist Alcohol consumption Alcohols Animal Model Animals Area Auditory Authorization documentation Autoradiography Behavior Behavior Therapy Behavioral Behavioral Mechanisms Binding Biological Brain CTOP Cell Line Child Cities Complex Congenital neurologic anomalies Control Animal Cues D-enkephalin Detection Development Disclosure Disease Dose Dysmorphology Environment Environmental Risk Factor Esthesia Ethanol FOS gene Face Failure Female Fetal Alcohol Spectrum Disorder Gene Expression Growth Human Human Resources Individual Instruction Laboratories Last Name Laws Life Link Maternal Behavior Mediating Mental Health Methods Microinjections Modeling Mothers Names Nature Neonatal Neuraxis Neurobiology Opioid Performance Play Pregnancy Principal Investigator Printing Process Progress Reports Psychology Public Health Rattus Reaction Registries Research Personnel Research Project Grants Role Sensory Sensory Process Site Social Behavior Social Environment Social Interaction Societies South Carolina Structure Symptoms System Techniques Testing Time Translating Universities Visual Woman Work alcohol exposure base cysteinyltyrosine experience human embryonic stem cell immunocytochemistry immunoreactivity medical schools mu opioid receptors neurobiological mechanism neuromechanism postnatal prenatal programs pup relating to nervous system research study response social somatosensory

项目摘要

DESCRIPTION (provided by applicant): Fetal alcohol spectrum disorder (FASD) includes a constellation of symptoms and deficits in social behavior has become acknowledged as possibly one of the most debilitating symptoms. However, the behavioral and neural mechanism giving rise to the social deficits seen in FASD and the degree to which the environment plays a role in these social deficits remains unknown. Thus, the environment of alcohol-exposed pups will be modified such that they are exposed to intensive normal social interactions during development, isolation during the juvenile period, and abnormal mothering behavior in order to examine mitigating or exacerbating factors in the social deficits. Interactions of environment will be examined across different doses of alcohol, with the prediction that effects of low doses of alcohol will be more sensitive to environmental manipulations. Based on evidence from this laboratory and others, it is hypothesized that the ethanol-induced social deficits might arise from changes in mu opioid system. This hypothesis is examined using autoradiography and microinjection techniques. Behavioral analyses of the social deficits observed in animals exposed to alcohol during development has demonstrated that the deficits are not likely due to changes in social motivation and some evidence suggests that there are deficits in the ability to process social cues. The social response of animals to different gradations of sensory cues and the ability to detect social cues in the olfactory, auditory and somatosensory domains will be examined. Using the additive factors method, the contribution of deficits in social cue processing to social deficits in general in ethanol-exposed animals will be determined. c-Fos immunoreactivity will be used to examine the neural structures contributing to the sensory processing deficit. The rat model of FASD used in this proposal entails exposure during both the prenatal and postnatal period, mimicking the effect of alcohol exposure during all three trimesters in the humans. FASD continues to be a public health problem occurring large expenses both to society and the individual. The proposed studies will use a rat model of FASD to delineate the behavioral and neurobiological mechanism underlying the social deficits in this disorder and the contribution of social environments to the impact of ethanol during development. These findings can then be translated into both biological and behavioral treatments for FASD.

描述（由申请人提供）：胎儿酒精谱系障碍（FASD）包括一系列症状和社会行为缺陷，已被公认为可能是最使人衰弱的症状之一。然而，导致 FASD 社交缺陷的行为和神经机制以及环境在这些社交缺陷中发挥作用的程度仍然未知。因此，暴露于酒精的幼崽的环境将被改变，使它们在发育过程中暴露于密集的正常社会互动，在幼年期被隔离，以及异常的母性行为，以检查减轻或加剧社会缺陷的因素。将检查不同剂量酒精与环境的相互作用，并预测低剂量酒精的影响将对环境操纵更加敏感。根据该实验室和其他实验室的证据，推测乙醇引起的社交缺陷可能是由于 mu 阿片系统的变化引起的。使用放射自显影和显微注射技术检验了这一假设。对发育过程中暴露于酒精的动物所观察到的社交缺陷的行为分析表明，这些缺陷不太可能是由于社交动机的变化造成的，并且一些证据表明处理社交线索的能力存在缺陷。将检查动物对不同等级的感觉线索的社会反应以及在嗅觉、听觉和体感领域检测社会线索的能力。使用加性因素方法，将确定暴露于乙醇的动物中社交线索处理缺陷对一般社交缺陷的贡献。 c-Fos 免疫反应性将用于检查导致感觉处理缺陷的神经结构。本提案中使用的胎儿酒精谱系障碍 (FASD) 大鼠模型需要在产前和产后期间暴露，模拟人类在所有三个三个月期间暴露于酒精的影响。胎儿酒精谱系障碍（FASD）仍然是一个公共卫生问题，给社会和个人带来巨大的损失。拟议的研究将使用 FASD 大鼠模型来描绘这种疾病的社会缺陷背后的行为和神经生物学机制，以及社会环境对发育过程中乙醇影响的贡献。这些发现可以转化为 FASD 的生物和行为治疗。