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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|Broadwater, Margaret A; Liu, Wen; Crews, Fulton T et al. (2014) Persistent loss of hippocampal neurogenesis and increased cell death following adolescent, but not adult, chronic ethanol exposure. Dev Neurosci 36:297-305|
|Lee, Joohwi; Lyu, Ilwoo; Styner, Martin (2014) Multi-atlas segmentation with particle-based group-wise image registration. Proc SPIE Int Soc Opt Eng 9034:903447|
|Qin, Liya; Crews, Fulton T (2014) Focal thalamic degeneration from ethanol and thiamine deficiency is associated with neuroimmune gene induction, microglial activation, and lack of monocarboxylic acid transporters. Alcohol Clin Exp Res 38:657-71|
|Ehlers, C L; Liu, W; Wills, D N et al. (2013) Periadolescent ethanol vapor exposure persistently reduces measures of hippocampal neurogenesis that are associated with behavioral outcomes in adulthood. Neuroscience 244:1-15|
|Vetreno, Ryan P; Qin, Liya; Crews, Fulton T (2013) Increased receptor for advanced glycation end product expression in the human alcoholic prefrontal cortex is linked to adolescent drinking. Neurobiol Dis 59:52-62|
|Qin, Liya; Liu, Yuxin; Hong, Jau-Shyong et al. (2013) NADPH oxidase and aging drive microglial activation, oxidative stress, and dopaminergic neurodegeneration following systemic LPS administration. Glia 61:855-68|
|Ehlers, Cindy L; Oguz, Ipek; Budin, Francois et al. (2013) Peri-adolescent ethanol vapor exposure produces reductions in hippocampal volume that are correlated with deficits in prepulse inhibition of the startle. Alcohol Clin Exp Res 37:1466-75|
|Qin, Liya; Crews, Fulton T (2012) NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration. J Neuroinflammation 9:5|
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