Education:
B.S., Psychology; Computer Science: University of Alabama, Birmingham
M.S., Experimental Psychology: Auburn University
Ph.D., Behavioral Pharmacology: Auburn University

Summary Statement:
The goals of our research are to 1) discover the neural circuits and molecular mechanisms that mediate the reinforcing and pleasurable subjective effects of alcohol and other drugs; 2) identify the long-term effects of cocaine and alcohol abuse during adolescence; and 3) identify novel neural targets and validate pharmacological compounds that may be used to treat problems associated with alcohol and drug abuse. Our studies have shown that the limbic system and extended amygdala regulate alcohol-seeking behavior and conditioned discriminative stimulus effects of alcohol. We established that neuropeptide-Y in the hypothalamus modulates excessive alcohol drinking similar to its role in obesity via the Y1 receptor, and that NPY-Y5 receptor blockade reduces the reinforcing effects of alcohol. Also, using gene knockout mice, we have shown that Protein Kinase C - epsilon regulates alcohol drinking, reinforcement, sensitivity, withdrawal, and mesolimbic dopamine release through enhancement of GABA-A receptor function. Other studies have shown that adolescent exposure to cocaine leads to enhanced vulnerability to the rewarding effects of cocaine during adulthood in mice via activation of the limbic system.

Representative Publications:
1.1. 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.