Clyde W. Hodge, Ph.D.

Email: chodge@med.unc.edu

Office Phone: (919) 843-4823

Education:

B.S., Psychology and Computer Science, University of Alabama, Birmingham

M.S., Experimental Psychology, Auburn University

Ph.D., Behavioral Pharmacology, Auburn University

Research Interests:

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 movement 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.

Research Projects:

Molecular Mechanisms of Ethanol Reinforcement
R01 AA014983; Hodge (PI)
The primary goal of this application is to characterize the involvement of metabotropic glutamate receptors in alcohol's reinforcing effects.

Molecular Mechanisms of Alcohol Drinking and Relapse
P60 AA011605; Component of UNC-CH Center Grant; Crews (PI), Hodge (Component PI) 
This component of the NIAAA Alcohol Center Grant is focused on elucidating the functional involvement of the cell signaling pathways in alcohol drinking and relapse.  Studies are focused on protein kinase C isoforms, the ERK/MAPK pathway, and how changes in activity of these kinases regulate alcohol drinking, relapse, and reinforcement.    

Behavioral and Molecular Mechanisms of Ethanol-Induced Depression 
R01 AA16629; Hodge (PI)
We have discovered that abstinence from chronic alcohol drinking is associated with increased depression-like behavior in mice. The goals of this multidisciplinary project are to identify molecular mechanisms of this alcohol-induced increase in depression.  

Mentored Research Projects:

Novel Mechanism of Ethanol Discrimination
K01 AA016009; Dr. Joyce Besheer (PI), Hodge (Mentor)
The primary goal of this project is to characterize neurobiological mechanisms of the subjective (i.e., discriminative) effects of alcohol.

Representative Publications:

1.    Hodge CW, Mehmert KK, Kelley SP, McMahon T, Haywood A, Olive MF, Wang D, Sanchez-Perez AM, Messing RO: Supersensitivity to allosteric GABA(A) receptor modulators and alcohol in mice lacking PKCepsilon. Nature Neuroscience 2:997-1002, 1999.

2.    Olive MF, Mehmert KK, Messing RO, Hodge CW: Reduced operant ethanol self-administration and in vivo mesolimbic dopamine responses to ethanol in PKCepsilon-deficient mice. European Journal of Neuroscience 12:4131-4140, 2000.

3.    Kelley SP, Nannini MA, Bratt AM, Hodge CW: Neuropeptide-Y in the paraventricular nucleus increases ethanol self-administration. Peptides 22:515-522, 2001.

4.    Olive MF, Mehmert KK, Nannini MA, Camarini R, Messing RO, Hodge CW. Deletion of the epsilon isoform of protein kinase C results in reduced ethanol withdrawal severity and altered withdrawal-induced expression of c-fos expression in various regions of the mouse brain. Neuroscience 103:171-179; 2001.

5.    Hodge CW, Raber J, McMahon T, Walter H, Sanchez-Perez AM, Olive MF, Mehmert K, Morrow AL, Messing RO: Decreased anxiety-like behavior, reduced stress hormones, and neurosteroid supersensitivity in mice lacking protein kinase Cepsilon. J Clin Invest 110:1003-1010, 2002.