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.
| Chen, Ziping; Hu, Dechun; Chen, Xingwu et al. (2017) Templated Sphere Phase Liquid Crystals for Tunable Random Lasing. Nanomaterials (Basel) 7: |
| Samudio-Ruiz, Sabrina L; Allan, Andrea M; Sheema, Sheema et al. (2010) Hippocampal N-methyl-D-aspartate receptor subunit expression profiles in a mouse model of prenatal alcohol exposure. Alcohol Clin Exp Res 34:342-53 |
| Samudio-Ruiz, Sabrina L; Allan, Andrea M; Valenzuela, Carlos Fernando et al. (2009) Prenatal ethanol exposure persistently impairs NMDA receptor-dependent activation of extracellular signal-regulated kinase in the mouse dentate gyrus. J Neurochem 109:1311-23 |
