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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：
7741745
负责人：
Sandra J Kelly
金额：
$ 39.61万
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 2012-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7741745
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(申请人提供)：胎儿酒精谱系障碍(FASD)包括一系列症状，社会行为缺陷已被公认为可能是最令人虚弱的症状之一。然而，导致FASD社会缺陷的行为和神经机制以及环境在这些社会缺陷中所起的作用程度仍不清楚。因此，暴露在酒精中的幼崽的环境将被改变，使它们在发育期间暴露于密集的正常社会互动中，在青少年时期处于孤立状态，以及不正常的育儿行为，以检查社会缺陷中的缓解或加剧因素。环境的相互作用将通过不同剂量的酒精进行检查，预测低剂量酒精的影响将对环境操纵更加敏感。根据本实验室和其他实验室的证据，推测酒精引起的社会缺陷可能是由于Mu阿片系统的变化引起的。这一假设通过放射自显影和显微注射技术进行了验证。对在发育过程中接触酒精的动物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，一些证据表明，处理社交线索的能力存在缺陷。将考察动物对不同等级的感觉线索的社会反应，以及在嗅觉、听觉和躯体感觉领域探测社会线索的能力。使用加性因子法，将确定在酒精暴露的动物中，社会线索处理缺陷对一般社会缺陷的贡献。C-Fos免疫反应将被用来检查导致感觉处理缺陷的神经结构。这项建议中使用的FASD大鼠模型在出生前和出生后都需要暴露，模拟人类在所有三个三个月期间酒精暴露的影响。FASD仍然是一个公共卫生问题，对社会和个人都造成了巨大的损失。这项拟议的研究将使用FASD的大鼠模型来描述这种障碍中潜在的社会缺陷的行为和神经生物学机制，以及社会环境对酒精在发育过程中的影响的贡献。然后，这些发现可以转化为FASD的生物和行为治疗。