Prenatal alcohol exposure: persistent damage to intracellular signaling pathways

描述（由申请人提供）：相关性：越来越多的证据表明，母亲在怀孕期间即使摄入适量酒精，其子女也可能出现认知和行为缺陷（Streissguth等人，1990年; Streissguth等人，1994年; Willford等人，2004年）。我们的产前酒精暴露小鼠模型提供了一种方法来研究在子宫内暴露于适量酒精的哺乳动物后代的认知缺陷。因为已知在传统的学习范例之后促分裂原活化蛋白激酶/细胞外信号调节激酶ERK 1/2的活化对于学习过程是必不可少的（阿特金斯等人，1998年，Blum等人，1999年，Selcher等人，1999年，Shalin等人，2004年）由于适度的产前酒精暴露导致的这种信号通路激活的缺陷可能是与以下相关的认知缺陷的一个潜在原因：子宫内中度酒精暴露了解产前诱导的认知缺陷的机制可能有助于克服这个问题。

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.