Prenatal alcohol exposure: persistent damage to intracellular signaling pathways

产前酒精暴露：细胞内信号通路持续受损

• 批准号: 7320950
• 负责人: Sabrina Leigh Samudio-Ruiz
• 金额: $ 2.73万
• 依托单位: UNIVERSITY OF NEW MEXICO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2009-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7320950
• 关键词: Adult; Adult Children; Affect; Alcohol consumption; Alcohols; Behavioral; Binding Proteins; Biological Assay; Brain; Bypass; Calcium; Child; Cognitive; Cognitive deficits; Congenital Abnormality; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Cyclic AMP-Responsive DNA-Binding Protein; D Aspartate; Data; Elements; Ethanol; Event; Extracellular Signal Regulated Kinases; Fetal Alcohol Exposure; Fire - disasters; Gene Expression; Glutamates; Goals; Hippocampus (Brain); Image; Immunoblotting; Impaired cognition; Impairment; In Vitro; Lead; Learning; MAPK1 gene; Mediating; Memory; Mental Retardation; Messenger RNA; Mitogen-Activated Protein Kinases; Mothers; Mus; N-Methyl-D-Aspartate Receptors; N-Methylaspartate; Neurons; Numbers; Phosphorylation; Pregnancy; Process; Protein Biosynthesis; Protein Kinase C; Receptor Activation; Response Elements; Saccharin; School-Age Population; Series; Signal Pathway; Signal Transduction; Slice; Synaptic Receptors; Synaptic Vesicles; Synaptic plasticity; Techniques; Transcriptional Regulation; Woman; alcohol exposure; fetal; in utero; long term memory; mature animal; mouse model; prenatal; prenatal exposure

DESCRIPTION (provided by applicant): Relevance: There is increasing evidence showing that both cognitive and behavioral deficits can occur in children whose mothers consumed even moderate amounts of alcohol during pregnancy (Streissguth et al. 1990, Streissguth et al. 1994, Willford et al. 2004). Our mouse model of prenatal alcohol exposure provides a way to study cognitive deficits in mammalian offspring exposed to moderate amounts of alcohol in utero. Because activation of the mitogen activated protein kinase/extracellular signal regulated kinase ERK1/2 following traditional learning paradigms is known to be essential to the learning process (Atkins et al. 1998, Blum et al. 1999, Selcher et al. 1999, Shalin et al. 2004) deficits in the activation of this signaling pathway due to moderate prenatal alcohol exposure could possibly be one underlying reason for the cognitive deficits associated with moderate ethanol exposure in utero. Understanding the mechanisms underlying prenatal induced cognitive deficits could help to overcome this issue.

描述(由申请人提供)：相关性：越来越多的证据表明，母亲在怀孕期间甚至适度饮酒的儿童可能会出现认知和行为缺陷(Streissguth等人)。1990年，Streissguth等人提出。1994年，Willford et al.2004年)。我们的胎儿期酒精暴露的小鼠模型为研究在子宫中暴露于中等剂量酒精的哺乳动物后代的认知缺陷提供了一种方法。因为遵循传统学习范式的丝裂原活化蛋白激酶/细胞外信号调节激酶ERK1/2的激活对学习过程是必不可少的(Atkins等人。1998年，Blum et al.1999年，Selcher et al.1999年，Shalin等人。(2004)胎儿期中度酒精暴露导致的这一信号通路激活缺陷可能是宫内中度酒精暴露导致认知障碍的一个潜在原因。了解孕期导致认知缺陷的机制有助于克服这一问题。