ArticleAddiction neuroscience2024
Voluntary adolescent alcohol exposure does not robustly increase adulthood consumption of alcohol in multiple mouse and rat models.
Article in Addiction neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Alcohol drinking sex-dependently regulates interleukin-1 pro-inflammatory signaling in the prefrontal cortex of mice and rhesus macaques.Brain, behavior, and immunity · 2026Article
- Chronic Alcohol Drinking Impairs Recognition Memory And Insulin-Associated Genes In The Medial Prefrontal Cortex.Molecular neurobiology · 2025Article
- Sex-specific effects of chronic alcohol consumption across the lifespan in the transgenic Alzheimer's Disease (TgF344-AD) rat model.Brain, behavior, and immunity · 2025Article
- Adolescent alcohol consumption alters sex-specific behaviors associated with prefrontal functional connectivity in mice.bioRxiv : the preprint server for biology · 2025Article
- Alcohol consumption confers lasting impacts on prefrontal cortical neuron intrinsic excitability and spontaneous neurotransmitter signaling in the aging brain in mice.Neurobiology of aging · 2025Article
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14 authors.
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Abstract
Adolescence is a period of increased risk taking, including increased alcohol and drug use. Multiple clinical studies report a positive relationship between adolescent alcohol consumption and risk of developing an alcohol use disorder (AUD) in adulthood. However, few preclinical studies have attempted to tease apart the biological contributions of adolescent alcohol exposure, independent of other social, environmental, and stress factors, and studies that have been conducted show mixed results. Here we use several adolescent voluntary consumption of alcohol models, conducted across four labs in three institutes and with two rodent species, to investigate the ramifications of adolescent alcohol consumption on adulthood alcohol consumption in controlled, pre-clinical environments. We consistently demonstrate a lack of robust increases in adulthood alcohol consumption. This work highlights that risks seen in both human datasets and other murine drinking models may be due to unique social and environmental factors - some of which may be unique to humans.
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