Hodge 2015Professor
Department of Psychiatry
Bowles Center for Alcohol Studies

Office | 3019A Thurston-Bowles Bldg, CB#7178
Email | chodge@med.unc.edu
Lab Website | Hodge Lab
Biographical Sketch

Research Interest

Alcoholism is a complex neuropsychiatric disorder that is characterized by recurring cycles of chronic drinking, abstinence and relapse. Emerging evidence suggests that alcohol and other drugs of abuse may produce maladaptive changes in a variety of neurotransmitter, cell signaling and gene transcription pathways that lead to enduring changes in brain structure and function. These neuroadaptations are thought to regulate behavioral pathologies that occur in alcoholism.

The primary goals of our research are to 1) elucidate neuroadaptations in molecular signaling pathways associated with chronic voluntary alcohol drinking and abstinence; and 2) investigate the functional involvement of these molecular pathways in the behavioral effects of alcohol including self-administration, mood regulation (i.e., anxiety and depression), discrimination, and sensitization. Understanding the molecular mechanisms of drug-induced plasticity in brain and behavioral functions is of potential importance for development of new pharmacotherapies for problems associated with alcoholism, such as relapse.

A major focus of our work is on understanding how alcohol alters neural processes to gain control over the individual via alterations of positive reinforcement mechanisms. Using rodent models, we have identified specific neural systems that regulate alcohol-seeking behavior and evaluate co-morbid neuropsychiatric conditions such as anxiety and depression. Recently, we have utilized unbiased high-throughput proteomic screens, to discover the spectrum of neural proteins that are altered by alcohol use by adults and adolescents. Protein targets in specific brain regions are validated for functional involvement in alcohol self-administration using site-specific microinjection strategies. At the mechanistic level, our studies have identified glutamate-linked receptors (e.g., NMDA, mGluR5, AMPA) and associated signaling pathways (e.g., PKC, ERK, CaMKII) as key targets of that regulate alcohol reinforcement. Recently, we have incorporated optogenetics and electrophysiological measures in our studies via training and collaboration within the UNC Alcohol Center Core, of which Dr. Hodge is the Director. By delineating how alcohol alters protein networks that, in turn, regulate drug-seeking behavior, we hope to elucidate novel neural mechanisms that influence the development of addiction.

Recent Publications

Click for a list of publications from PubMed

Cannabinoid CB1 receptor inhibition blunts adolescent-typical increased binge alcohol and sucrose consumption in male C57BL/6J mice. Agoglia AE, Holstein SE, Eastman VR, Hodge CW. Pharmacol Biochem Behav. 2016 Apr;143:11-7. doi: 10.1016/j.pbb.2016.01.009. PMID:26800788

Potentiation of amygdala AMPA receptor activity selectively promotes escalated alcohol self-administration in a CaMKII-dependent manner. Cannady R, Fisher KR, Graham C, Crayle J, Besheer J, Hodge CW. Addict Biol. 2016 Jan 6. doi: 10.1111/adb.12357. [Epub ahead of print. PMID:26742808

CaMKII inhibition in the prefrontal cortex specifically increases the positive reinforcing effects of sweetened alcohol in C57BL/6J mice. Faccidomo S, Reid GT, Agoglia AE, Ademola SA, Hodge CW. Behav Brain Res. 2016 Feb 1;298(Pt B):286-90. doi: 10.1016/j.bbr.2015.11.018. PMID:26608538

Moderate Alcohol Drinking and the Amygdala Proteome: Identification and Validation of Calcium/Calmodulin Dependent Kinase II and AMPA Receptor Activity as Novel Molecular Mechanisms of the Positive Reinforcing Effects of Alcohol. Salling MC, Faccidomo SP, Li C, Psilos K, Galunas C, Spanos M, Agoglia AE, Kash TL, Hodge CW. Biol Psychiatry. 2016 Mar 15;79(6):430-42. doi: 10.1016/j.biopsych.2014.10.020. PMID:25579851

CaMKIIα-GluA1 Activity Underlies Vulnerability to Adolescent Binge Alcohol Drinking. Agoglia AE, Holstein SE, Reid G, Hodge CW. Alcohol Clin Exp Res. 2015 Sep;39(9):1680-90. doi: 10.1111/acer.12819. PMID:2624762