1. Neonatal Ethanol Exposure Causes Behavioral Deficits in Young Mice
- Author
-
Wenhua Xu, Lu Dai, Jia Luo, Gang Chen, Susan Barron, Jacqueline A. Frank, Andrew B. Hawkey, Howard H. Brim, and Hui Li
- Subjects
Male ,0301 basic medicine ,Elevated plus maze ,Offspring ,Central nervous system ,Medicine (miscellaneous) ,Morris water navigation task ,Physiology ,Motor Activity ,Toxicology ,Article ,Open field ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Medicine ,Maze Learning ,reproductive and urinary physiology ,Sex Characteristics ,Fetus ,Behavior, Animal ,Ethanol ,business.industry ,Age Factors ,Ethanol exposure ,Psychiatry and Mental health ,030104 developmental biology ,Brain growth ,medicine.anatomical_structure ,Female ,business ,030217 neurology & neurosurgery - Abstract
Background Fetal ethanol (EtOH) exposure can damage the developing central nervous system and lead to cognitive and behavioral deficits, known as fetal alcohol spectrum disorders (FASD). EtOH exposure to mouse pups during early neonatal development was used as a model of EtOH exposure that overlaps the human third-trimester "brain growth spurt"-a model that has been widely used to study FASD in rats. Methods C57BL/6 male and female mice were exposed to EtOH (4 g/kg/d) on postnatal days (PD) 4 to 10 by oral intubation. Intubated and nontreated controls were also included. Behavioral testing of the offspring, including open field, elevated plus maze, and Morris water maze, was performed on PD 20 to 45. Results EtOH exposure during PD 4 to 10 resulted in hyperactivity and deficits in learning and memory in young mice with no apparent sex differences. Conclusions Based on these data, this neonatal intubation mouse model may be useful for future mechanistic and genetic studies of FASD and for screening of novel therapeutic agents.
- Published
- 2018
- Full Text
- View/download PDF