The primary objective of this NADIA core is to integrate and expand the Consortium research projects. The hypothesis of the Scientific Core is that adolescent intermittent ethanol (AIE) impacts brain development and induces specific neuro-adaptations that persist into adulthood as a specific neurochemical and morphological phenotype. Thus, the Scientific Core will serve and link NADIA components by providing neurochemical and morphological brain atlases that will define the phenotype of the brain exposed to alcohol during adolescence. Each component will send brains to the core for immunohistochemical determination of pivotal neurotransmitter gene expression in brain regions related to the physiology and behaviors being studied. Additionally, Magnetic Resonance Imaging (MRI) and Diffusion Tensor Imaging (DTI) data will be collected on select data sets in order to provide global structural information on the impact of different AIE models on adult brain. Finally, all the resulting data will be shared and unused brain tissue will be archived to allow for future analysis. Together, these approaches will provide critical information on neurobiological mechanisms that underlie AlE-induced changes in adult behavior and physiology. The Scientific Core will use an animal model of adolescence alcohol drinking to investigate how alcohol changes brain structure and neurochemistry. This endeavor, along with the resulting data repository, serves to integrate the research components of the NADIA Consortium and will provide a foundation for understanding differences in adolescent life trajectories and maturation of important behavioral repertoires.
The Scientific Core will use an animal model of adolescence alcohol drinking to investigate how alcohol changes brain structure and neurochemistry. This endeavor, along with the resulting data repository, serves to integrate the research components of the NADIA Consortium and will provide a foundation for understanding differences in adolescent life trajectories and maturation of important behavioral repertoires.
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|Sakharkar, Amul J; Vetreno, Ryan P; Zhang, Huaibo et al. (2016) A role for histone acetylation mechanisms in adolescent alcohol exposure-induced deficits in hippocampal brain-derived neurotrophic factor expression and neurogenesis markers in adulthood. Brain Struct Funct 221:4691-4703|
|Vetreno, Ryan P; Yaxley, Richard; Paniagua, Beatriz et al. (2016) Diffusion tensor imaging reveals adolescent binge ethanol-induced brain structural integrity alterations in adult rats that correlate with behavioral dysfunction. Addict Biol 21:939-53|
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|Lee, Joohwi; Kim, Sun Hyung; Styner, Martin (2016) Multi-Object Model-based Multi-Atlas Segmentation for Rodent Brains using Dense Discrete Correspondences. Proc SPIE Int Soc Opt Eng 9784:|
|Crews, Fulton T; Vetreno, Ryan P (2016) Mechanisms of neuroimmune gene induction in alcoholism. Psychopharmacology (Berl) 233:1543-57|
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|Vetreno, Ryan P; Crews, Fulton T (2015) Binge ethanol exposure during adolescence leads to a persistent loss of neurogenesis in the dorsal and ventral hippocampus that is associated with impaired adult cognitive functioning. Front Neurosci 9:35|
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