Abstract
Adolescent binge alcohol exposure has long-lasting effects on the expression of hypothalamic genes that regulate the stress response, even in the absence of subsequent adult alcohol exposure. This suggests that alcohol can induce permanent gene expression changes, potentially through epigenetic modifications to specific genes. Epigenetic modifications can be transmitted to future generations therefore, and in these studies we investigated the effects of adolescent binge alcohol exposure on hypothalamic gene expression patterns in the F1 generation offspring. It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences compared to offspring from alcohol-naïve parents. Specifically, major differences were observed in the expression of genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure.
Highlights
Several decades of research have established that maternal alcohol consumption during critical periods of fetal brain development leads to devastating long-term consequences on cognitive function and social behavior
Greater than 90% of alcohol consumed by youth is achieved through ‘‘binge’’ drinking, which is defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as consuming enough alcohol in two hour period to raise the blood alcohol concentration (BAC) above the 0.08% legal driving limit
Global Microarray Analysis We used a genome-wide microarray approach to determine the effects of parental adolescent binge EtOH exposure on transgenerational (F1, EtOH naıve) gene expression in the hypothalamus
Summary
Several decades of research have established that maternal alcohol consumption during critical periods of fetal brain development leads to devastating long-term consequences on cognitive function and social behavior. Less is known about the consequences of parental alcohol consumption, outside of gestational periods, on alcohol-dependent epigenetic modifications that could subsequently manifest as detrimental phenotypic changes in the offspring. Greater than 90% of alcohol consumed by youth is achieved through ‘‘binge’’ drinking, which is defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as consuming enough alcohol in two hour period to raise the blood alcohol concentration (BAC) above the 0.08% legal driving limit. Binge drinking during adolescence has been linked with a greater risk for alcoholism, drug abuse, depression, and suicide [7]
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