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Neonatal Ethanol Exposure Causes Behavioral Deficits in Young Mice
Author(s) -
Xu Wenhua,
Hawkey Andrew B.,
Li Hui,
Dai Lu,
Brim Howard H.,
Frank Jacqueline A.,
Luo Jia,
Barron Susan,
Chen Gang
Publication year - 2018
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13598
Subject(s) - morris water navigation task , offspring , open field , fetal alcohol syndrome , elevated plus maze , medicine , fetus , water maze , anesthesia , physiology , ethanol , pregnancy , psychology , hippocampus , biology , psychiatry , anxiety , biochemistry , genetics
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 C57 BL /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.