Plasticity in the PFC Following 5-7-9 Postnatal Alcohol Exposure Using Exercise as an Intervention

Abstract

Fetal alcohol spectrum disorder (FASD) is an umbrella term used
to describe the wide range of deficits caused by exposure to alcohol
in utero. Lack of restraint from conducting a behavior or a
psychological process, is often impaired in these individuals
(inhibition). One region that is attributed to this lack of inhibition is
the medial prefrontal cortex. GABAergic parvalbumin interneurons
(PV+) play a role in the inhibition surrounding neurons in the
medial prefrontal cortex. Therefore, we hypothesize that alcohol
exposed individuals will have less PV+ cells compared to their
control counterparts. This study used C57/6J male adolescent
mice. These subjects were divided into two groups, alcohol exposure
(20% ethanol solution at 5 g/kg) or saline. Behavioral testing
occurred between PD72-79. Subjects were tested on the Passive
Avoidance task and Rotarod. On 85 PD mice were anesthetized,
perfused using saline, and the brains processed using Parvalbumin
antibody. Preliminary results show a decrease in PV+ cells in
alcohol exposed subjects compared to control groups. Further,
alcohol exposed subjects exhibited an increased latency to learn
the passive avoidance task. Both the number of PV+ cells and
the level of inhibitory control were decreased with prenatal alcohol
exposure infer the differences in inhibition between the
groups; can be seen by quantity of the PV+ cells in the medial
prefrontal cortex. These results show the long term impact prenatal
alcohol exposure have on the functioning and anatomy of
the medial prefrontal cortex.