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，即使母亲在怀孕期间饮酒适量，其孩子也可能出现认知和行为缺陷（Streissguth et al. 1990, Streissguth et al. 1994, Willford et al. 2004）。我们的小鼠产前酒精暴露模型为研究哺乳动物后代在子宫内暴露于适量酒精的认知缺陷提供了一种方法。由于已知有丝分裂原激活的蛋白激酶/细胞外信号调节激酶ERK1/2的激活遵循传统的学习范式对学习过程至关重要（Atkins等人1998年，Blum等人1999年，Selcher等人1999年，Shalin等人2004年），由于适度产前酒精暴露导致的该信号通路激活缺陷可能是与子宫内适度酒精暴露相关的认知缺陷的一个潜在原因。了解产前诱导的认知缺陷的潜在机制可以帮助克服这一问题。

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.