UTHSCSA Faculty Profiles v1.0

Ginsburg, Brett C. PhD

School of Medicine
Psychiatry
(210) 567-0871
ginsburg@uthscsa.edu

My research program focuses on the behavioral neurobiology of alcohol, opioids, and cannabinoids. Through this research, I have established myself as a leading preclinical investigator of behavioral mechanisms involved in successful alcoholism recovery, as well as a leading expert on synthetic cannabinoids (a troubling new class of abused substances). My research program has been supported by extramural funding from several agencies, including the National Institutes of Health, the Department of Defense, and private donors.


My research on alcohol (supported by numerous awards from the National Institute of Alcohol and Alcoholism and an endowment by a private donor) has established among the very first animal models of recovery. My results indicate that longer periods of recovery, modeled by reinforcing alternative behavior, results in behavior which is more resistant to disruption by events or experiences that often prompt relapse. This is consistent with human research showing that the risk of relapse declines with longer periods of successful recovery, and intuitively that once recovery becomes a habit and replaces the old habit of substance use, relapse becomes less likely. A currently funded project is examining whether prior ethanol exposure slows the transition of recovery into a habit that replaces substance use, and whether cognitive enhancing medications might speed this transition. If confirmed, these medications could be used as adjuncts to behavioral therapy to make recovery more resilient earlier in treatment, helping to decrease all too common relapse during this particularly vulnerable time.


Previously, I published several well-cited studies on the ability of the anti-smoking medication varenicline and the selective serotonin reuptake inhibitor (SSRI) fluvoxamine to reduce alcohol use, particularly in the context of ongoing alternative behavior. I reported that the ability of these (and other) medications to reduce drinking while sparing the alternative behavior depends on the baseline pattern of these behaviors. The implication of this finding is that these medications might be more effective in people with high levels of drinking relative to other activities (the most severely afflicted), but might increase drinking among more moderate drinkers who have greater balance with other daily activities. Indeed, several recently published clinical trials using SSRIs are consistent with this conclusion. Combining my expertise in preclinical evaluation of potential anti-alcoholism medications with preclinical models of recovery provides a unique way to improve our understanding of and treatment strategies for alcoholism.


My research on cannabinoids has been supported by an R03 from the National Institute on Drug Abuse and by an award from the Department of Defense. This research focused on the rising problem of synthetic cannabinoids, which are legally available and have led to a troubling number of emergency room admissions. My research has demonstrated that synthetic cannabinoids exert similar behavioral effects to the primary psychoactive constituent in cannabis, but because they are pharmacologically more powerful, they may produce more frequent adverse effects than cannabis. I found that administration of a cannabinoid antagonist can rescue mice from synthetic cannabinoid overdose, which suggests that providing first responders with such a medication could help the increasingly common cases of human synthetic cannabinoid overdose.


I have also examined aspects of opioid use disorder, using similar strategies to those I employ in my ethanol research. In research finded by the Department of Defense, I found that when given an easily accessible alternative, behavioral allocation shifted from opioid use to alternative behavior. When this behavior no longer produced the alternative, rats reallocate their behavior and resume opioid use. These results suggest that stressors similar to daily life frustrations might prompt a relapse, but that this phenomenon is better conceptualized in terms of behavioral allocation rather than a physiological result of the stressor itself.

9/2013 - Present Associate Professor UTHSCSA, Psychiatry, San Antonio, TX