THE IMPACT OF NEONATAL ALCOHOL EXPOSURE AND VOLUNTARY EXERCISE ON CHOLINERGIC FIBER LENGTH AND CG2 VOLUME IN THE RAT MEDIAL PREFRONTAL CORTEX
Date
2019-05
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
University of Delaware
Abstract
Prenatal alcohol exposure is known to cause chronic behavioral impairment
and neurocognitive deficits diagnosed as Fetal Alcohol Spectrum Disorders (FASD).
With a prevalence of one in every twenty children affected by prenatal alcohol
exposure in the United States, FASD remains a serious public health concern. This
study uses a rodent model of FASD to investigate the effects of third trimesterequivalent
alcohol exposure and adolescent exercise intervention on the underexplored
cortical-projecting pathway of the central cholinergic system, the nucleus basalis of
Meynert (NBM)-cortical pathway. Recent literature has found that neonatal choline
supplementation following prenatal alcohol exposure may ameliorate some alcoholinduced cognitive deficits, but the structural basis of these functional changes has not yet been investigated. Therefore, the current study examines cholinergic fiber length
along the NBM-cortical cholinergic pathway and Cg2 volume of the medial prefrontal
cortex (mPFC) in our experimental paradigm. Alcohol exposed (AE) male Long-
Evans pups received ethanol in a binge-like manner (5.25 g/kg/day) twice a day during
postnatal day (PD) 4-9. Control groups consisted of sham-intubated (SI) and suckle
control (SC) rats. Pups were weaned on PD23 and socially housed in same-sex groups
of three. Wheel running (WR) rats had 24-hour voluntary access to a running wheel
from PD30-72. All animals were sacrificed on PD72 and forebrain tissue was
collected and histochemically stained via a Hedreen and Bacon modified Karnovsky-
Roots method to visualize acetylcholinesterase (AChE)-positive fibers in Cg2.
Overall, there was no significant effect of postnatal treatment or behavioral
intervention on cholinergic fiber length or Cg2 volume in adulthood. No significant
interactions were observed. These data indicate that cholinergic axons are innervating
their mPFC target region in adulthood. Future investigation is necessary to elucidate
cellular cholinergic mechanisms affected by neonatal alcohol exposure that may be
contributing to the observed PFC-dependent cognitive deficits characteristic of FASD.
Description
Keywords
Neonatal alcohol exposure, Voluntary exercise, Cholinergic fiber length, CG2 volume