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Sustained Impairments in Brain Insulin/IGF Signaling in Adolescent Rats Subjected to Binge Alcohol Exposures during
Alexandra Ewenczyk1, Jason Ziplow1, Ming Tong1
1Departments of Pathology (Neuropathology), Neurology, Neurosurgery & Medicine and the Liver Research Center, Rhode Island Hospital and the Warren Alpert Medical School at Brown University, Providence, RI.
Early ethanol exposure in rats caused lasting motor deficits and cerebellar damage by disrupting insulin and IGF-1 signaling pathways critical for brain development.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Fetal alcohol spectrum disorder (FASD) results from prenatal ethanol exposure, causing neurodevelopmental deficits.
- While perinatal defects are linked to impaired brain insulin/IGF signaling, sustained adolescent effects remain unclear.
Purpose of the Study:
- To investigate if early postnatal binge ethanol exposure impacts adolescent cerebellar structure, function, and insulin/IGF signaling.
- To assess neurobehavioral outcomes and molecular changes in young adolescent rats.
Main Methods:
- Rats received binge ethanol or saline via injection on postnatal days 2, 4, 6, and 8.
- Motor function was tested using rotarod on P19-20.
- Cerebella were analyzed for histological, molecular, and biochemical markers on P30.
Main Results:
- Ethanol exposure led to impaired motor function and persistent cerebellar hypocellularity.
- Reduced expression of neuronal and oligodendrocyte genes was observed.
- Deficits in insulin/IGF signaling, including receptor binding and Akt/GSK-3β pathways, were significant.
Conclusions:
- Sustained inhibition of insulin/IGF-1 signaling may underlie FASD-related neurobehavioral and structural abnormalities in adolescents.
- This signaling is crucial for cell survival, neuronal plasticity, and myelin maintenance in the developing brain.
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