Browsing by Author "Lungwitz, Elizabeth A."

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    Brain response in heavy drinkers during cross-commodity alcohol and money discounting with potentially real rewards: A preliminary study
    (Elsevier, 2023-07-06) Lungwitz, Elizabeth A.; Dzemidzic, Mario; Shen, Yitong I.; Plawecki, Martin H.; Oberlin, Brandon G.; Psychiatry, School of Medicine
    Background: Alcohol use disorder (AUD) is associated with exaggerated preference for immediate rewards, a candidate endophenotype for use disorders. Addiction symptomology is often well-described by the preference for immediate intoxication over other delayed prosocial rewards. We measured brain activation in AUD-implicated regions during a cross-commodity delay discounting (CCD) task with choices for immediate alcohol and delayed money. Methods: Heavy drinkers (n=24) experienced a brief intravenous alcohol infusion prime, regained sobriety, then chose between 'One Shot' and delayed money in an adjusting delay CCD task (sober and intoxicated); also during fMRI (sober). Participants also performed a behavioral sensation seeking task and completed self-report inventories of other risk factors. We assessed brain activation to choices representing immediate intoxication versus delayed money rewards in a priori regions of interest defined within the framework of Addictions NeuroImaging Assessment. Results: Activation to CCD choice versus control trials activated paralimbic and ventral frontal cortical regions, including orbital and medial prefrontal cortex, posterior cingulate/retrosplenial cortex, angular and superior frontal gyri. We detected no differences between immediate or delayed choices. Left medial orbitofrontal cortex activation correlated with alcohol-induced wanting for alcohol; females showed greater activation than males. Behavioral sensation seeking correlated with right nucleus accumbens task engagement. Conclusions: Alcohol decision-making elicited activation in regions governing reward, introspection, and executive decision-making in heavy drinkers, demonstrating the utility of laboratory tasks designed to better model real-world choice. Our findings suggest that the brain processes subserving immediate and delayed choices are mostly overlapping, even with varied commodities.
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    THE COGNITIVE OVERRIDE OF ANXIETY IS ACCOMPLISHED BY SOCIAL FAMILIARITY AND IS MEDIATED BY THE MEDIAL PREFRONTAL CORTEX.
    (Office of the Vice Chancellor for Research, 2012-04-13) Lungwitz, Elizabeth A.; Sanghani, Sahil; Harvey, Brian; Bah, Alhussein; Dietrich, Amy; Truitt, William A.
    In rats, social familiarity can alleviate anxiety-like behavior observed in the social interaction test. We propose that a neural circuit that includes the medial Prefrontal Cortex (mPFC) and Basolateral Amygdala (BLA), in which the mPFC processes social cues of familiarity and suppresses BLA outputs that lead to anxiety-like behavior, regulate this social familiarity effect. To investigate the effect of social familiarity on anxiety, we developed the Social Interaction-Habituation (SI-h) paradigm, consisting of a 5 min social interaction test repeated daily with the experimental rat exposed to the same partner rat on each test day. As the experimental rat becomes “familiar” with the partner rat, a significant increase in SI time is observed by day 5 compared to day 1, producing a SI-familiarity effect (SI-f). This SI-f effect is dependent on the presence of an anxiogenic stimulus (bright light), and familiarity to a partner rat. No increases in SI times were observed in rats when the SI-h test was performed under dark conditions or when exposed to novel partners on days 1-5. After establishing SI-f, exposure to a novel partner significantly reduces SI times, suggesting the SI-f effect is a result of recognition of the familiar partner rat. Re-exposure to the original partner in a new environment produces an enhanced SI-f effect; SI time significantly increases from day 1 by day 3. Bilateral inhibition of the mPFC with a GABAA agonist blocks the anxiolytic SI-f effect. Exposure to the same partner 24 hours following mPFC inhibition, SI times increase significantly higher than day 1. These data indicate that the mPFC activity is necessary for expression of the SI-f effect.
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    Psychosocial impairment following mild blast-induced traumatic brain injury in rats
    (Elsevier, 2021) Race, Nicholas S.; Andrews, Katharine D.; Lungwitz, Elizabeth A.; Vega Alvarez, Sasha M.; Warner, Timothy R.; Acosta, Glen; Cao, Jiayue; Lu, Kun-Han; Liu, Zhongming; Dietrich, Amy D.; Majumdar, Sreeparna; Shekhar, Anantha; Truitt, William A.; Shi, Riyi; Anatomy, Cell Biology and Physiology, School of Medicine
    Traumatic brain injury (TBI) is associated with increased risk for mental health disorders, impacting post-injury quality of life and societal reintegration. TBI is also associated with deficits in psychosocial processing, defined as the cognitive integration of social and emotional behaviors, however little is known about how these deficits manifest and their contributions to post-TBI mental health. In this pre-clinical investigation using rats, a single mild blast TBI (mbTBI) induced impairment of psychosocial processing in the absence of confounding physical polytrauma, post-injury motor deficits, affective abnormalities, or deficits in non-social behavior. Impairment severity correlated with acute upregulations of a known oxidative stress metabolite, 3-hydroxypropylmercapturic acid (3-HPMA), in urine. Resting state fMRI alterations in the acute post-injury period implicated key brain regions known to regulate psychosocial behavior, including orbitofrontal cortex (OFC), which is congruent with our previous report of elevated acrolein, a marker of neurotrauma and 3-HPMA precursor, in this region following mbTBI. OFC of mbTBI-exposed rats demonstrated elevated mRNA expression of metabotropic glutamate receptors 1 and 5 (mGluR1/5) and injection of mGluR1/5-selective agonist in OFC of uninjured rats approximated mbTBI-induced psychosocial processing impairment, demonstrating a novel role for OFC in this psychosocial behavior. Furthermore, OFC may serve as a hotspot for TBI-induced disruption of psychosocial processing and subsequent mental health disorders.