Victoria Macht

I am an Assistant Professor of Psychology at the University of North Carolina Wilmington, where I teach and mentor students in behavioral neuroscience, developmental psychology, and psychoneuroimmunology. I earned my Ph.D. in Experimental Psychology from the University of South Carolina under the guidance of Drs. Lawrence Reagan and Sandra Kelly where I focused on neurological and behavioral deficits in models of fetal alcohol spectrum disorders and Gulf War Illness. I completed my postdoctoral training at the Bowles Center for Alcohol Studies at the University of North Carolina at Chapel Hill under the mentorship of Fulton Crews, where I spearheaded projects examining how adolescent alcohol exposure impacted learning and memory-related circuits through long-term activation of innate immune systems. My path into neuroscience has been shaped by a passion for understanding how the brain adapts—or sometimes fails to adapt—when challenged by stressors such as alcohol, early-life adversity, or immune activation at various points across the lifespan.

At UNCW, I work closely with undergraduates and graduate students on projects exploring the intersections of the immune system, hippocampal circuitry, and behavior. Mentoring is one of the most rewarding aspects of my role. I strive to cultivate curiosity, critical thinking, and technical skills that empower students to pursue their own scientific questions and career goals.

Education

Ph.D. in Experimental Psychology, University of South Carolina.
M.A. in Experimental Psychology, University of South Carolina.
B.S. in Psychology, Furman University.

Research Interests

My lab bridges behavioral neuroscience, developmental neurobiology, and psychoneuroimmunology to uncover how psychological and pharmacological insults recalibrate the interface between our nervous system and our immune system across the lifespan to impact learning and memory related behaviors. One of the major players that my lab investigates in compromising these systems is adolescent alcohol exposure. Binge alcohol exposure across adolescent development initiates long-lasting innate immune responses—notably through danger-associated molecules like HMGB1—resulting in microglial activation, suppressed hippocampal neurogenesis, and altered neuronal architecture. The result is long-lasting remodeling of hippocampal circuitry - a brain region critical for learning and memory-related processes - that compromises spatial learning, memory consolidation, and cognitive flexibility.

We utilize a variety of techniques to accomplish these aims, including immunohistochemistry, electrophysiology, and behavior. This three-pronged approach allows us to ask if insults like alcohol cause (1) structural, (2) physiological, and (3) functional deficits in hippocampal circuitry. For behavioral analysis, paradigms such as the Morris and radial arm water mazes enable the dissection of multiple components of performance: not only hippocampal-dependent spatial learning, but also procedural learning, motivation, and strategy use. This multidimensional view helps clarify whether deficits arise from true cognitive impairments or from altered drive and task execution.