Moderate chronic fetal alcohol exposure causes a motor learning deficit in adult outbred Swiss-Webster mice

Abstract

Prenatal ethanol exposure can negatively affect development, causing physical and/or cognitive deficits in the offspring. Behavioral changes are typically characterized during childhood, but they can also persist into adulthood. The extent of Fetal Alcohol Spectrum Disorder (FASD) abnormalities depends upon the amount and manner of ethanol intake, leading to a large variety of animal models. In order to mimic the genetically diverse human condition, we examined an outbred strain of mice exposed to chronic gestational ethanol and characterized subsequent behavioral alterations during adulthood. To detect deficits in cognitive ability and/or motor function, we ran the mice through tests designed to detect either memory/learning ability or motor strength/skill. We tested cognitive responses using the Barnes Maze and the Open Field Aversion Test, and motor skills using Kondziela's Inverted Screen Test and the rotarod. As adults, the FASD mice showed no significant differences on grip strength, open field, or the Barnes maze; however, we found that outbred mice who had experienced moderate prenatal ethanol exposure were slower to learn the rotarod as adults, though they did not differ in overall performance. Our data suggest a specific FASD vulnerability in motor learning ability, and also open the door to further investigation on the effect of ethanol on brain areas involved in motor learning, including the striatum.

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder

“…Recent research supports the hypothesis that sex-specific effects in white matter regions exist in models of FASD. For instance, studies have demonstrated sex-specific effects of EtOH on spatial and motor learning (Goodlett & Peterson, 1995;Reekes et al, 2016), a oligodendrogenesis-dependent task (Xiao et al, 2016), and sex-specific deficits in eye movement have been detected in FASD subjects (Paolozza, Munn, Munoz, & Reynolds, 2015), potentially resulting from optic nerve hypoplasia following developmental EtOH exposure, characterized by abnormal myelin integrity (Parson, Dhillon, Findlater, & Kaufman, 1995;Pinazo-Duran, Renau-Piqueras, Guerri, & Str€ omland, 1997). Although beyond the scope of this investigation, it will be important in future studies to determine the impact of sex as a biological variable in our mouse model,…”