WHAT WE'RE WORKING ON

Work in the Crowley Lab focuses on understanding behavioral and physiological brain states involved in a variety of neuropsychiatric disorders, such as anxiety and addiction. We use a combination of behavioral, electrophysiological, imaging, and genetic approaches to inform the basic science of disease etiology, treatment, and prevention. Our overarching focus is on neuropeptidergic modulation of discrete neural circuits and systems.

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SOMATOSTATIN PEPTIDERGIC SIGNALING IN THE PREFRONTAL CORTEX

FUNDED BY NIAAA R21AA028088, NARSAD YOUNG INVESTIGATOR GRANT (BRAIN AND BEHAVIOR RESEARCH FOUNDATION) 

Alcoholism and major depressive disorder (MDD) are highly comorbid disorders, both of which are major health and social concerns—costing the US a combined $300 billion each year. Homeostatic perturbations in neuronal systems are thought to underlie both alcoholism and MDD, and interestingly, important sex differences are seen in both diseases, with women being more likely to suffer depression and more likely to suffer from the negative long-term consequences of drinking. 

 

Intervention strategies that target specific brain regions or groups of neurons holds the promise of treatments with fewer side effects, resulting in greater adherence to treatment and fewer social complications. In order to create such treatments, the field needs a deeper understanding of the brain regions and even specific neurons within the region. Funded by the Penn State Social Science Research Institute, this project seeks to identify, in both mice and humans, the role of specific types of neurons in the overlapping etiology of depression and alcohol addiction in both males and females. 

Ongoing work in the lab combines optogenetics, chemogenetics, behavior, and electrophysiology to understand how stomatostatin neurons throughout the brain may play a role in binge drinking.

Collaborators: 

Dr. Patrick Drew, College of Engineering, PSU

ADOLESCENT ALCOHOL INDUCED CHANGES IN PFC FUNCTIONING

FUNDED BY THE BINGHAMTON UNIVERSITY DEVELOPMENTAL EXPOSURE TO ALCOHOL RESERACH CENTER (DEARC) P50 AWARD (P50AA017823)

Alcohol consumption has a multitude of negative consequences for the brain, and these effects are exacerbated with adolescent alcohol exposure, with binge alcohol consumption being chiefly prevalent and problematic (Bava & Tapert, 2010; Silveri, 2012). The animal literature has provided a breadth of information on the negative consequences of adolescent alcohol exposure (Spear, 2000). Adolescent mice that undergo the Drinking in the Dark (DID) binge-like model of alcohol consumption show significantly higher consumption of alcohol as compared to adults (Holstein, Spanos, & Hodge, 2011).  Behaviorally, intermittent ethanol exposure during both early (post-natal day, PND 24-45) and late (PND 45-65) adolescence has been shown to alter anxiety-like behavior in both male and female mice (Varlinskaya, Hosová, Towner, Werner, & Spear, 2020). Neurologically, adolescent alcohol exposure has been shown to cause altered intrinsic excitability of both pyramidal neurons and fast-spiking GABA neurons in the prelimbic (PL) cortex (Salling et al., 2018; Trantham-Davidson et al., 2016). Together, this work all points to profound and precise alterations in neuronal signaling and behavior following adolescent alcohol exposure. However, the role of, and alterations of, specific neuronal and peptidergic populations has not been thoroughly uncovered. Ongoing work on this project seeks to understand how adolescent alcohol consumption rewires signaling in the PL cortex - and what the longterm ramifications of these changes are. 

Collaborators:

Dr. Terrance Deak, Behavioral Neuroscience, Binghamton University (DEARC P50 Center Director)

INVESTIGATION OF KEY OPIOID PATHWAYS MODULATED BY ADOLESCENT CHRONIC VARIABLE STRESS

FUNDED BY THE NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM, THE CLINICAL AND TRANSLATIONA SCIENCES INSTITUTE, THE SOCIAL SCIENCE RESEARCH INSTITUTE, AND THE CONSORTIUM TO COMBAT SUBSTANCE ABUSE

Adolescent stress is a key risk factor for drug abuse in adulthood. Though many maladaptive and drug-addiction related outcomes following stress are known, it is unclear precisely how the brain is altered following stress to escalate drug addiction. Accumulating evidence indicates that adolescent stress causes changes in the developing limbic and cortical structures in the brain, regions heavily involved in the progression of drug intake to drug abuse. This project outlines the consequences of adolescent stress on the brain's neurotransmitter systems and their interactions with opioid receptors.

Collaborators:

Dr. Helen Kamens, College Health and Human Development, PSU

Dr. Kevin Alloway,  College of Medicine, PSU

Dr. Bruce Gluckman, College of Engineering, PSU

Dr. Matt Hearing, Marquette University