Abstract
Adolescent binge drinking represents a major public health challenge and lead to persistent psychiatric disorders. However, the underlying pathogenic mechanisms remain poorly understood. Myelin abnormalities were observed in human subjects with alcohol abuse. Gray matter myelination in the prefrontal cortex and hippocampus during adolescence are vulnerable to alcohol.In the present study, we investigated whether myelin abnormalities in the gray matter are involved in behavioral abnormalities induced by adolescent binge ethanol treatment (ABET). To produce ABET, C57BL/6J mouse was given EtOH (3.0g/kg, i.e. 25% ethanol w/v) once a day during adolescence (P28-46) in an intermittent fashion. ABET persistently developed behavioral abnormalities such as anxiety-like behaviors in the marble burying test and the novelty suppressed feeding test, impaired memory function in the novel object recognition test, and impairments of social behavior in social interaction test. ABET decreased myelin-related protein and oligodendrocyte lineage cells in the prefrontal cortex and hippocampus. Clemastine, which promotes oligodendroglial differentiation and myelination, rescues the behavioral abnormalities. These findings suggest that myelin abnormalities in the gray matter may be involved in the behavioral abnormalities caused by ABET in adulthood.
