Clyde Hodge, Ph.D.
Department of Psychiatry
Bowles Center for Alcohol Studies
Office | 3019A Thurston-Bowles Bldg, CB#7178
Email | email@example.com
Lab Website |
The Hodge laboratory is focused on understanding the neural mechanisms of alcohol-seeking behavior. The primary goal of our research is to identify and validate neural targets (e.g., receptors, kinases, transcription factors, and neural circuits) of alcohol that mechanistically control alcohol reinforcement (e.g., alcohol-seeking behavior) and other behavioral pathologies associated with alcohol use disorder. In other words, we are investigating how alcohol hijacks brain and behavioral processes to produce addiction.
To accomplish this goal, we employ state-of-the-art computer-controlled operant alcohol self-administration methods that are complemented by a variety of rodent behavioral measures of cognition, anxiety, motor behavior, and reward. Behavioral methods are coupled with site-specific brain microinjection, immunohistochemical and immunoblot techniques, proteomic methods, gene knockout, and viral vector strategies that allow us to define brain regions and pathways that the mediate reinforcing effects of alcohol. At the neurochemical level, our work is focused on the role of amino acid neurotransmitters, such as glutamate with emphasis on mGluR5 and AMPA receptor subtypes. We also focus on cell signaling kinases (ERK MAPK, CaMKII, PKC) that mediate long-term neurobehavioral adaptations to ethanol. At the neural circuit level, we have made seminal discoveries of how dopamine, GABA, glutamate receptors, cell signaling systems, within mesolimbic circuits (VTA, accumbens, amygdala, hypothalamus, and frontal cortex) regulate alcohol’s reinforcing effects.
Mining the nucleus accumbens proteome for novel targets of alcohol self-administration in male C57BL/6J mice. Faccidomo S, Swaim KS, Saunders BL, Santanam TS, Taylor SM, Kim M, Reid GT, Eastman VR, Hodge CW. Psychopharmacology. 2018; 235(6):1681-1696. NIHMSID: NIHMS947885 PubMed [journal] PMID: 29502276, PMC5949261
Cue-induced reinstatement of alcohol-seeking behavior is associated with increased CaMKII T286 phosphorylation in the reward pathway of mice. Salling MC, Hodge CJ, Psilos KE, Eastman VR, Faccidomo SP, Hodge CW Pharmacology, biochemistry, and behavior. 2017; 163:20-29. NIHMSID: NIHMS935215 PubMed [journal] PMID:29100991
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. Addiction biology. 2017; 22(3):652-664. NIHMSID: NIHMS748206 PubMed [journal] PMID: 26742808