Trainees

Emily Atkinson, PhD
Postdoctoral Fellow, Fridberg Lab
Broadly, my research aims to identify modifiable risk factors for the onset and maintenance of problematic substance use and substance use disorders to aid in the development of effective interventions. I am specifically interested in using intensive longitudinal methods, such as ecological momentary assessment, to study the relationship between heightened emotional states, trait-level emotion-based risk factors, and hazardous drinking behavior.

Anahi Bustillos Salazar
PhD Student, Xu Lab
Substance use disorders remain a global health crisis with no FDA-approved treatments. My research focuses on understanding how autophagy proteins in dopamine neurons regulate cocaine reward behaviors. Specifically, I investigate how autophagy molecules influence and control cocaine induced reward behavior by modulating dopamine D2 receptor degradation. Using genetic knockout models, pharmacological interventions, and behavioral assays, I aim to characterize the molecular mechanisms underlying cocaine addiction. This work could potentially identify novel therapeutic targets for treating cocaine use disorder and preventing relapse.

Hanna Carmon, PhD
Postdoctoral Fellow, Groman Lab
Individual differences in responses to Pavlovian reward cues and in adaptive decision-making, the process of updating behavior when contingencies change, are hypothesized to be strongly implicated in vulnerability to addiction. Although these behavioral patterns are well characterized, the developmental and potential neuroimmune processes that shape them remain poorly understood. My research integrates behavioral assays with developmental neuroimmune analyses to determine how early-life microglial maturation influences variation in decision-making and responses to reward-predictive cues. By identifying how neuroimmune and developmental microglial mechanisms give rise to these behavioral traits, this work seeks to uncover biological pathways that shape susceptibility to addiction-related behaviors.

Benjamin Clites, PhD
Postdoctoral Fellow, Barreiro Lab & Green Lab
Pro-inflammatory pathways, and microglial inflammation in particular, have been heavily implicated in the risk and development of alcohol use disorder (AUD) & problem drinking. While some pro-inflammatory molecules and pathways in AUD have been identified (e.g. TNF-alpha, NF-kB), many other upstream & parallel genetic interactors have not been. My work aims to use high-throughput CRISPR screens of thousands of genes in human-induced pluripotent stem cells (hiPSCs) to identify novel regulators of ethanol-induced microglial activation in an unbiased fashion. Because I aim to use single-cell transcriptomics as well as functional phenotypes (e.g. phagocytosis, gross morphology) to assess the consequences of gene perturbations, we will learn how these perturbations echo throughout the whole transcriptome. These insights will help to identify a suite of novel genes and pathways as candidate targets to ameliorate ethanol-induced microglial activation, and hopefully, the transition to addiction and problematic drinking.

Raymond Ruiz, PhD
Postdoctoral Fellow, King Lab
My research interests include identifying, understanding, and addressing risk factors for the continued use of nicotine and tobacco products. Additionally, my research uses a strength-based approach to identify protective factors that can be leveraged to assist with cessation attempts. I am particularly interested in targeting cessation treatments for priority populations to better meet their cessation needs, and to enhance accessibility, acceptability, and effectiveness.

Yuexi Yin, PhD
Postdoctoral Fellow, McGehee Lab
While opioids are effective for pain relief, they carry serious adverse side effects including dependence and tolerance. My research focuses on identifying novel pain control mechanisms to support the development of safer, non-opioid pain therapies. Specifically, I use fiber photometry, pharmacological interventions, and behavioral assays, to investigate how acetylcholine receptors modulate pain signaling within the ventrolateral periaqueductal gray, a central hub in the descending pain pathway.