Overview: Molecular and Cellular Pathogenesis in Alcoholism. The UNC NIAAA Alcohol Research Center (ARC) fosters interdisciplinary collaborative research on alcoholism, alcohol abuse and the impact of alcohol on health and disease - exactly the goal of an NIAAA ARC. The UNC Bowles Center for Alcohol Studies (CAS) provides a foundation of administrative support and dedicated space for alcohol research. Across ARC components molecular signaling, synaptic networks, neurocircuitry and psychopathology are investigated in models of binge drinking. The scope of these studies requires the Center mechanism to integrate the multiple signaling systems and neurocircuits that underlie complex addiction-like behaviors. The UNC ARC is a catalyst of discovery that promotes collaboration, expands use of new methods and scientific knowledge through regular research meetings, scientific seminars, core research services, annual clinical conferences, pilot projects and through stimulation of interest in the effects of alcohol on health across the University and State. Training and mentoring of students and junior faculty contribute to scholarly interactions and successful laboratory research programs through the ARC. Health professional and youth curricula promote interest in science and knowledge that contribute to improved health. The ARC synergizes with existing investigator funding to promote interactions among multidisciplinary investigators focused on molecular mechanisms of ethanol-related behavioral and tissue pathology. The ARC Specific Aims are to investigate mechanisms of alcohol-induced behavioral, molecular, cellular and neural circuit pathogenesis and to disseminate information on alcohol to health professionals and youth. Research components investigate hypotheses on ethanol-induced regulation of signaling kinases, receptor expression and trafficking, cytokine and peptide gene induction, changes in brain networks and circuitry as well as alcohol induced mood, behavior and drug taking as addiction-like behavioral pathologies. By conducting focused investigations that integrate molecular signaling mechanisms across neural networks and neurocircuitry, the ARC creates synergies that promote and catalyze discoveries. This ARC proposal continues a research focus on molecular and cellular mechanisms with a new emphasis on dysfunctional brain networks and neurocircuitry, a theme at the cutting edge of neuroscience. The ARC will conduct, promote, support, and mentor research on alcoholic pathology and educate broad groups of health professionals and youth in North Carolina.

Public Health Relevance

Alcoholism is a major public health problem of unknown etiology. This ARC is devoted to understanding the mechanisms of pathology associated with alcoholism and alcohol abuse. The field has been hampered by lack of understanding of the brain circuitry that underlies alcohol-induced pathology. We propose a comprehensive and integrated investigation of molecular, cellular and circuit pathology in alcoholism using forefront strategies.

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Comprehensive Center (P60)
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Grandison, Lindsey
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University of North Carolina Chapel Hill
Schools of Medicine
Chapel Hill
United States
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Smith, Christopher T; Sierra, Yecenia; Oppler, Scott H et al. (2014) Ovarian cycle effects on immediate reward selection bias in humans: a role for estradiol. J Neurosci 34:5468-76
Sparta, Dennis R; Hovelsø, Nanna; Mason, Alex O et al. (2014) Activation of prefrontal cortical parvalbumin interneurons facilitates extinction of reward-seeking behavior. J Neurosci 34:3699-705
Coleman Jr, Leon Garland; Liu, Wen; Oguz, Ipek et al. (2014) Adolescent binge ethanol treatment alters adult brain regional volumes, cortical extracellular matrix protein and behavioral flexibility. Pharmacol Biochem Behav 116:142-51
Kietzman, Henry W; Everson, Joshua L; Sulik, Kathleen K et al. (2014) The teratogenic effects of prenatal ethanol exposure are exacerbated by Sonic Hedgehog or GLI2 haploinsufficiency in the mouse. PLoS One 9:e89448
Smith, Christopher T; Swift-Scanlan, Theresa; Boettiger, Charlotte A (2014) Genetic polymorphisms regulating dopamine signaling in the frontal cortex interact to affect target detection under high working memory load. J Cogn Neurosci 26:395-407
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
Jennings, Joshua H; Stuber, Garret D (2014) Tools for resolving functional activity and connectivity within intact neural circuits. Curr Biol 24:R41-50
Swift-Scanlan, Theresa; Smith, Christopher T; Bardowell, Sabrina A et al. (2014) Comprehensive interrogation of CpG island methylation in the gene encoding COMT, a key estrogen and catecholamine regulator. BMC Med Genomics 7:5
Cook, Jason B; Werner, David F; Maldonado-Devincci, Antoniette M et al. (2014) Overexpression of the steroidogenic enzyme cytochrome P450 side chain cleavage in the ventral tegmental area increases 3?,5?-THP and reduces long-term operant ethanol self-administration. J Neurosci 34:5824-34
Zou, Jian Y; Crews, Fulton T (2014) Release of neuronal HMGB1 by ethanol through decreased HDAC activity activates brain neuroimmune signaling. PLoS One 9:e87915

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