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Published on: August 5, 2017
Exercise in Adolescence Enhances Callosal White Matter Refinement in the Female Brain in a Rat Model of Fetal Alcohol
Katrina A Milbocker1, Ian F Smith1, Eric K Brengel1
1Department of Psychological and Brain Sciences, University of Delaware, Newark, DE 19716, USA.
Insights
Prenatal alcohol exposure causes Fetal Alcohol Spectrum Disorders (FASD), impacting white matter development. Exercise interventions show promise in improving oligodendrocyte differentiation in adolescent female rats with FASD.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Prenatal alcohol exposure affects 1 in 20 infants, leading to Fetal Alcohol Spectrum Disorders (FASD).
- FASD is associated with delayed cerebral white matter maturation, impairing cognitive functions.
- Previous research indicates alcohol's detrimental effects on oligodendrocyte development, particularly in the male brain.
Purpose of the Study:
- To investigate the impact of prenatal alcohol exposure on white matter development in the female brain.
- To examine the potential of adolescent exercise interventions to promote white matter recovery in FASD.
Main Methods:
- Utilized a rat model of Fetal Alcohol Spectrum Disorders (FASD).
- Assessed oligodendrocyte numbers and myelin basic protein production in the corpus callosum.
- Analyzed myelin-related gene expression and evaluated the effects of voluntary adolescent exercise.
Main Results:
- Prenatal alcohol exposure reduced mature oligodendrocytes and myelin basic protein in the female corpus callosum.
- Myelination timing in the female corpus callosum is inherently earlier, irrespective of postnatal treatment.
- Adolescent exercise intervention increased mature oligodendrocytes in alcohol-exposed female rats.
Conclusions:
- Oligodendrocyte differentiation is impaired but potentially recoverable in the adolescent female brain affected by FASD.
- Behavioral interventions like exercise may offer a therapeutic avenue for white matter deficits in FASD.
- This study highlights sex-specific vulnerabilities and recovery potentials in FASD-related white matter injury.
Abstract:
A total of 1 in 20 infants born annually are exposed to alcohol prenatally, which disrupts neurodevelopment and results in several disorders categorized under the umbrella term Fetal Alcohol Spectrum Disorders (FASD). Children and adolescents affected by FASD exhibit delayed maturation of cerebral white matter, which contributes to deficits in executive function, visuospatial processing, sensory integration, and interhemispheric communication. Research using animal models of FASD have uncovered that oligoglia proliferation, differentiation, and survival are vulnerable to alcohol teratogenesis in the male brain due in part to the activation of the neuroimmune system during gestation and infancy. A comprehensive investigation of prenatal alcohol exposure on white matter development in the female brain is limited. This study demonstrated that the number of mature oligodendrocytes and the production of myelin basic protein were reduced first in the female corpus callosum following alcohol exposure in a rat model of FASD. Analysis of myelin-related genes confirmed that myelination occurs earlier in the female corpus callosum compared to their counterparts, irrespective of postnatal treatment. Moreover, dysregulated oligodendrocyte number and myelin basic protein production was observed in the male and female FASD brain in adolescence. Targeted interventions that support white matter development in FASD-affected youth are nonexistent. The capacity for an adolescent exercise intervention to upregulate corpus callosum myelination was evaluated: we discovered that volunteer exercise increases the number of mature oligodendrocytes in alcohol-exposed female rats. This study provides critical evidence that oligoglia differentiation is difficult but not impossible to induce in the female FASD brain in adolescence following a behavioral intervention.
