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Fetal Alcohol Effects on Circadian clocks and POMC

胎儿酒精对生物钟和 POMC 的影响

基本信息

批准号：
7856010
负责人：
DIPAK KUMAR SARKAR
金额：
$ 6.39万
依托单位：
RUTGERS, THE STATE UNIV OF N.J.
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-07-20 至 2010-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7856010
关键词：
Adolescent Adult Affect Alcohol consumption Alcohols Animal Model Animals Behavioral Binding Proteins Biological Biological Clocks Biological Rhythm Cell Nucleus Child Chronic Circadian Rhythms Clinical Cyclic AMP Data Development Elements Endocrine Endorphins Estrogens Ethanol Exposure to Female Fetal Alcohol Exposure Fetal Alcohol Syndrome Fetal Tissues Fetal alcohol effects Fetus Gastrin releasing peptide Gene Expression Gene Proteins Gonadotropins Health Hormonal Human Hypothalamic structure Immunohistochemistry Lasers Lead Life Messenger RNA Microscopy Modeling Molecular Naltrexone Neuraxis Neurons Neurosecretory Systems Opioid Output Ovariectomy Pacemakers Pathology Pattern Perinatal Exposure Periodicity Phase Plasma Pro-Opiomelanocortin Proteins Radioimmunoassay Rattus Regulation Research Research Personnel Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Sleep Sleep Disorders Structure of nucleus infundibularis hypothalami Techniques Testing Therapeutic Time Western Blotting Withdrawal alcohol exposure beta-Endorphin biological systems circadian pacemaker depression drinking experience falls fetal laser capture microdissection male neonate offspring problem drinker protein expression response suprachiasmatic nucleus transmission process young adult

项目摘要

Exposure of a fetus to ethanol can lead to the development of fetal alcohol syndrome, which is characterized by various morphological and behavioral deficits in fetal alcohol-exposed (FAE) offspring. These offspring often show clinical sleep-wake disturbances and abnormalities in the functions of the neuroendocrine system. Recent studies have identified the possibility that the sleep-wake disturbances and neuroendocrine function abnormalities in the FAE offspring are related to long-term changes in circadian clock mechanisms. Employing the rat animal model, this proposal determines whether fetal exposure to ethanol causes long- lasting changes in the circadian output of beta-endorphin neurons located in the arcuate nucleus of the hypothalamus and their regulation of plasma gonadotropin release. It tests the hypothesis that fetal exposure to ethanol causes an abnormality in the adult expression of the central clock mechanisms in the suprachaismatic nucleus of the hypothalamus leading to alteration in the internal clock mechanisms and the phasic hormonal output of beta-endorphin neurons. It also identifies whether fetal exposure to ethanol alters the molecular mechanism governing the photic responses of the central and internal clocks. The proposed research uses laser-captured microscopy, immunohistochemistry, Western blot, radioimmunoassay, and real-time RT-PCR techniques to identify gene and protein expressions that are critically involved in the regulation of central and internal clock mechanisms and the phasic hormonal outputs from beta-endorphin neurons. The proposed studies should provide a better understanding of the long-term consequences of fetal exposure to ethanol in the circadian clock functions. This information should help to develop therapeutic strategies in managing sleep-wake disturbances and the resultant health consequences in FAE offspring.

胎儿暴露于乙醇可导致胎儿酒精综合征的发展，其特点是