Additional Contact Information:
Department of Biomedical Sciences
James H. Quillen College of Medicine
PO Box 70582
Johnson City, TN 37614
Office: Room 1-32, Bldg. 1
Phone: (423) 439-6297
FAX: (423) 439-2017
Assistant Professor, Department of Neuroscience, Medical University of South Carolina
2. Post Traumatic Stress Disorder
3. Adolescent Drug Use
The focus of my research laboratory is to use multiple approaches with translational implications to study the neuroanatomical adaptations that occur with alcohol use disorder (AUD). The majority of my work has emphasized the importance of glutamatergic processes in drug- and fear-related memories. For example, my laboratory has shown that the extinction of alcohol-seeking behavior can be facilitated with modulation of the mGlu5 receptor during extinction training (a model of exposure therapy in rodents). This treatment also reduced cued relapse of alcohol-seeking behavior (a model of drug relapse). Furthermore, we observed changes in both structural (increased dendritic spine density) and functional plasticity in the specific brain regions. There is high comorbidity between post-traumatic stress disorder (PTSD) and heavy alcohol use. Due to the overlap in the neural mechanisms that underlie drug and fear memories, a recent set of experiments from my lab has investigated the interactions between AUD and PTSD. I have found chronic exposure to alcohol leads to a persistent deficit in the extinction of previously acquired fear memories. My goal is to determine how alcohol exposure interacts with the neurocircuitry involved in the extinction and recall of fear-related memories. I am also part of the Neurobiology of Adolescent Drinking in Adulthood (NADIA) consortium that focuses on the impact of adolescent alcohol exposure in the adult rat. For example, we have shown that exposure to chronic alcohol during the adolescent period leads to a marked reduction in the ability to extinguish alcohol-seeking behavior in adulthood. Also, adolescent alcohol exposure can facilitate the learning of fear memories in adulthood, suggesting that it may contribute to the development of stress-related disorders. Ultimately, my lab uses a variety of techniques and behavioral models in rodents that can provide strong translational findings to disorders such as AUD and PTSD in humans.
R01 AA027706-01A1 Justin T. Gass (Co-PI)
Adolescent Alcohol Abuse, Traumatic Stress, and Vulnerability to Development of PTSD
Role: Co-Principal Investigator
The purpose of this project is to investigate the impact of adolescent alcohol abuse on cognitive behaviors in adulthood. It will also provide a better understanding of how traumatic events experienced during the adolescent period have lasting effects on future alcohol use, relapse-like behaviors, and reactivity to subsequent stressors.
R01 AA024526-01A1 Justin T. Gass (PI)
NIAAA Interactions Between Chronic Alcohol Exposure and Fear Memories
Role: Principal Investigator
The purpose of this project is to better understand the neural mechanisms that underlie the comorbid use of alcohol with PTSD. It will focus on the complex interactions of chronic alcohol exposure on the extinction of fear memories and the impact of fear-related cues on alcohol consumption. It will also examine the potential use of cognitive enhancers (e.g. mGlu5 positive allosteric modulator CDPPB) to facilitate the extinction of fear-related memories.
- Garcia-Keller, C., Smiley, C., Monforton, C., Melton, S., Kalivas P., & Gass, J.T. N-acetylcysteine Treatment During Acute Stress Prevents Stress- induced Augmentation of Addictive Drug Use and Relapse. In Press: Addiction Biology.
- Cannady, R., McGonigal, J.T., Newsom, R., Woodward, J.J., Mulholland, P.J., & Gass, J.T. (2017). Infralimbic cortex KCa2 channels regulate mGlu5- dependent plasticity and extinction of alcohol seeking behavior. Journal of Neuroscience, 37(16), 4359-4369. PMCID5413180.
- Macht, V.A., Wood, D., Kelly, S.J., & Gass, J.T. (2017). Sex-specific effects of developmental alcohol exposure on cocaine-induced place preference in adulthood. Behavioral Brain Research, 332: 259-268. PMCID5570610.
- Braunscheidel, K., Gass, J.T., Mulholland, P.J., Floresco, S.B., & Woodward, J.J. (2017). Persistent cognitive and morphological alterations induced by repeated exposure of adolescent rats to the abused inhalant toluene. Neurobiology of Learning & Memory, 144: 136-146, PMCID5583007.
- McGonigal, J.T., Chandler, L.J, & Gass, J.T. (2017). Deficits in the extinction of ethanol-seeking behavior following chronic intermittent ethanol exposure are attenuated with positive allosteric modulation of mGlu5. Neuropharmacology, 113, 198-205, PMCID5148675.
- Trantham-Davidson, H., Centanni, S.W., Garr, S.C., New, N.N., Mulholland, P.J., Gass, J.T., Glover, E.J., Fluoresce, S.B., Crews, F.T., Krishnan, H.R., Pandey, S.C., & Chandler, L.J. (2017). Binge-Like Alcohol Exposure during Adolescence Disrupts Dopaminergic Neurotransmission in the Adult Prelimbic Cortex. Neuropsychopharmacology, 42(5), 1024-1036. PMCID5506791.
- Gass, J.T., Trantham-Davidson, H.,Kassab, A.S., Olive, M.F., & Chandler, L.J. (2014). Enhancement of extinction learning attenuates ethanol- seeking behavior and alters plasticity within the addiction neurocircuitry. Journal of Neuroscience, 34(22), 7562-74. PMCID: 4035518.
- Gass, J.T., Glen, W.B., McGonigal, J.T., Trantham-Davidson, H., Lopez, M., Randall,
P.K., Yaxley, R., Floresco, S.B., & Chandler, L.J. (2014). Adolescent alcohol exposure
reduces behavioral flexibility, promotes disinhibition, and increases resistance to
extinction of ethanol self- administration in adulthood. Neuropsychopharmacology,
39(11), 2570-83. PMCID: 4207336 *Featured in NIAAA Spectrum Newsletter (February,
PubMed link to publications