NMDA RECEPTOR EXPRESSION AFTER FETAL ALCOHOL EXPOSURE

胎儿酒精暴露后 NMDA 受体的表达

• 批准号: 2893976
• 负责人: Kimberly Nixon
• 金额: $ 1.15万
• 依托单位: UNIVERSITY OF TEXAS AT AUSTIN
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-06-28 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2893976
• 关键词: NMDA receptors; alcoholism /alcohol abuse; apoptosis; behavioral /social science research tag; developmental psychology; embryo /fetus toxicology; ethanol; fetal alcohol syndrome; frustration; hippocampus; laboratory rat; learning; protein structure function; psychopharmacology; receptor expression; short term memory

ADHD, a widely diagnosed disorder in the school-aged population, is correlated with a variety of causes, but its etiology remains a mystery. Alcohol exposure during pregnancy has been correlated with the occurrence of ADHD in childhood. As ADHD may have several subtypes, one of which is the result of hippocampal dysfunction, and alcohol acts primarily on the hippocampus, alcohol-induced damage to the hippocampus may describe a subtype of ADHD. The project is also a further extension of the investigation of the effect of alcohol on the NMDA receptor, a primary receptor in the hippocampus. The project determines the composition of NMDA receptor protein subunits in rats exposed to alcohol during the third trimester equivalent and second and third trimesters combined. The secondary subunits of the NMDA modulate its function by altering Mg2+ affinity to the attached calcium channel, which in specific configurations may promote either excitotoxicity or apoptosis. Differential NMDA receptor function is observed after exposure to EtOH, as well as cell death, but the means by which cells die has not been described. This project seeks to answer whether altered NMDA receptor subunit composition is responsible for the change in NMDA receptor function, whether it causes apoptosis or excitotoxicity, and its subsequent effects on behavior.

ADHD是校际人口中被广泛诊断的疾病的ADHD，是 与各种原因相关，但其病因仍然是一个谜。 怀孕期间的酒精暴露与 童年时期的多动症发生。 由于多动症可能有几个子类型，一个 其中是海马功能障碍和酒精作用的结果 主要在海马，酒精引起的海马损害 可以描述多动症的亚型。 该项目也是进一步的扩展 研究酒精对NMDA受体的影响 海马中的一级受体。 该项目确定 暴露于酒精的大鼠中NMDA受体蛋白亚基的组成 在第三学期和第二和第三个三个月中 合并。 NMDA的二级亚基通过 改变MG2+对附件的亲和力，该通道在 特定的构型可能会促进兴奋性或凋亡。 暴露于EtOH后，观察到差异NMDA受体功能， 以及细胞死亡，但细胞死亡的手段没有 描述。该项目试图回答是否改变了NMDA受体 亚基组成负责NMDA受体的变化 功能，无论是引起凋亡还是兴奋性毒性及其 随后对行为的影响。