The Charleston Alcohol Research Center (ARC) continues to focus on treatment and treatment implications as an overarching theme. The ARC continues to embrace multidisciplinary and translational research approaches, integrating both basic research and clinical investigations all centered on this common theme. The ARC also continues its tradition of teaming junior faculty with more experienced investigators, capitalizing on new talent and bringing sophisticated cutting-edge technologies and research approaches that enhance research efforts in addressing the Center's overall scientific goals. The ARC is comprised of four research projects and three cores. The Administrative Core provides the leadership and infrastructure to facilitate the overall scientific and educational mission of the Center as a whole. The Shared Resource Core provides vital scientific services needed by Center researchers to facilitate integration, maximize resources, and increase productivity. The Pilot Project Core attracts new investigators and new ideas to the Center, thereby broadening and augmenting its research and training activities. In this renewal application, proposed preclinical and clinical research projects all center on a common research focus - neuroadaptations in cortical processes that underlie transition from controlled to uncontrolled drinking. Two basic research projects will use sophisticated circuitry mapping, and cellular and molecular biology techniques to examine how chronic alcohol exposure alters the function of cortical areas, projections and networks relevant to behavioral control and motivational effects of alcohol. This work will lay the critical foundation for future efforts to target these cortical-subcortical circuitry changes in developing new treatments. Two clinical research projects will employ sophisticated neuroimaging techniques to focus on similar cortical areas and projections in evaluating the ability of different treatment modalities (pharmacological and non- pharmacological) to alter the circuitry and reduce alcohol cue-induced brain activation, craving, and drinking. The Charleston ARC is poised to continue its national leadership role and demonstrated success in: (a) fostering multidisciplinary and translational state-of-the-art research efforts that are thematically-focused on the topic of treatment and treatment implications; (b) attracting new (especially early-stage) investigators into the Center, thereby invigorating its research efforts; and (c) providing a stimulating environment that enriches training opportunities and professional development for the next generation of researchers in the alcohol field.

Public Health Relevance

The Charleston Alcohol Research Center is dedicated to addressing one of the nation's foremost public health concerns: alcohol use disorders and alcoholism. The Center embraces a multidisciplinary, translational research approach involving both clinical and preclinical researchers who are investigating why some individual's transition from social drinking that can be controlled to more excessive, uncontrolled drinking. Understanding brain mechanisms involved in this transition to uncontrolled compulsive-like alcohol consumption is crucial for developing new and more effective therapeutic strategies for arresting the progression to alcohol addiction, and preventing negative consequences associated with alcohol use disorder.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Specialized Center (P50)
Project #
5P50AA010761-25
Application #
9843619
Study Section
Special Emphasis Panel (ZAA1)
Program Officer
Kwako, Laura Elizabeth
Project Start
1996-12-01
Project End
2020-12-31
Budget Start
2020-01-01
Budget End
2020-12-31
Support Year
25
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Medical University of South Carolina
Department
Psychiatry
Type
Schools of Medicine
DUNS #
183710748
City
Charleston
State
SC
Country
United States
Zip Code
29407
Anderson, Ethan M; Larson, Erin B; Guzman, Daniel et al. (2018) Overexpression of the Histone Dimethyltransferase G9a in Nucleus Accumbens Shell Increases Cocaine Self-Administration, Stress-Induced Reinstatement, and Anxiety. J Neurosci 38:803-813
Osterndorff-Kahanek, Elizabeth A; Tiwari, Gayatri R; Lopez, Marcelo F et al. (2018) Long-term ethanol exposure: Temporal pattern of microRNA expression and associated mRNA gene networks in mouse brain. PLoS One 13:e0190841
Stewart, Scott H; Reuben, Adrian; Anton, Raymond F (2018) Reply: Carbohydrate Deficient Transferrin in Patients with Cirrhosis: A Tale of Bridges. Alcohol Alcohol 53:351-352
Kearney-Ramos, Tonisha E; Lench, Daniel H; Hoffman, Michaela et al. (2018) Gray and white matter integrity influence TMS signal propagation: a multimodal evaluation in cocaine-dependent individuals. Sci Rep 8:3253
Haun, Harold L; Griffin, William C; Lopez, Marcelo F et al. (2018) Increasing Brain-Derived Neurotrophic Factor (BDNF) in medial prefrontal cortex selectively reduces excessive drinking in ethanol dependent mice. Neuropharmacology 140:35-42
Schacht, Joseph P; Voronin, Konstantin E; Randall, Patrick K et al. (2018) Dopaminergic Genetic Variation Influences Aripiprazole Effects on Alcohol Self-Administration and the Neural Response to Alcohol Cues in a Randomized Trial. Neuropsychopharmacology 43:1247-1256
McGuier, Natalie S; Rinker, Jennifer A; Cannady, Reginald et al. (2018) Identification and validation of midbrain Kcnq4 regulation of heavy alcohol consumption in rodents. Neuropharmacology 138:10-19
Nimitvilai, Sudarat; Lopez, Marcelo F; Woodward, John J (2018) Effects of monoamines on the intrinsic excitability of lateral orbitofrontal cortex neurons in alcohol-dependent and non-dependent female mice. Neuropharmacology 137:1-12
Dowdle, Logan T; Brown, Truman R; George, Mark S et al. (2018) Single pulse TMS to the DLPFC, compared to a matched sham control, induces a direct, causal increase in caudate, cingulate, and thalamic BOLD signal. Brain Stimul 11:789-796
Zamudio-Bulcock, Paula A; Homanics, Gregg E; Woodward, John J (2018) Loss of Ethanol Inhibition of N-Methyl-D-Aspartate Receptor-Mediated Currents and Plasticity of Cerebellar Synapses in Mice Expressing the GluN1(F639A) Subunit. Alcohol Clin Exp Res 42:698-705

Showing the most recent 10 out of 209 publications