@article {11154,
	title = {Dissecting brain networks underlying alcohol binge drinking using a systems genomics approach.},
	journal = {Molecular Neurobiology},
	volume = {56},
	year = {2019},
	pages = {2791-2810},
	abstract = {Alcohol\&nbsp;use disorder (AUD) is a complex psychiatric disorder with strong genetic and environmental risk factors. We studied the molecular perturbations\&nbsp;underlying\&nbsp;risky\&nbsp;drinking\&nbsp;behavior by measuring transcriptome changes across the neurocircuitry of addiction in a genetic mouse model of\&nbsp;binge\&nbsp;drinking. Sixteen generations of selective breeding for high blood\&nbsp;alcohol\&nbsp;levels after a\&nbsp;binge\&nbsp;drinking\&nbsp;session produced global changes in\&nbsp;brain\&nbsp;gene expression in\&nbsp;alcohol-na{\"\i}ve High\&nbsp;Drinking\&nbsp;in the Dark (HDID-1) mice. Using gene expression profiles to generate circuit-level hypotheses, we developed a\&nbsp;systems\&nbsp;approach\&nbsp;that integrated regulation of gene coexpression\&nbsp;networks\&nbsp;across multiple\&nbsp;brain\&nbsp;regions, neuron-specific transcriptional signatures, and knowledgebase analytics. Whole-cell, voltage-clamp recordings from nucleus accumbens shell neurons projecting to the ventral tegmental area showed differential ethanol-induced plasticity in HDID-1 and control mice and provided support for one of the hypotheses. There were similarities in gene\&nbsp;networks\&nbsp;between HDID-1 mouse brains and postmortem brains of human alcoholics, suggesting that some gene expression patterns associated with high\&nbsp;alcohol\&nbsp;consumption are conserved across species. This study demonstrated the value of gene\&nbsp;networks\&nbsp;for data integration across biological modalities and species to study mechanisms of disease.},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459809/},
	author = {Ferguson, LB and Zhang, L and Kircher, D and Wang S, and Mayfield, R D and Crabbe, JC and Morrisett, RA and Harris, R A and Ponomarev, I.}
}
