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Julie A. Carlsten Christianson, PhD

Julie Carlsten Christianson portrait
Professor, Anatomy and Cell Biology
jchristianson@kumc.edu

Professional Background

Dr. Julie Christianson is a Professor in the departments of Anatomy and Cell Biology and Anesthesiology at the University of Kansas Medical Center. Her research is focused on understanding the influence of early life stress on the development of comorbid chronic pain and affective disorders later in life. Her ongoing NIH-funded work is focused on using pharmacological or voluntary exercise intervention to abrogate the long-term effects of early life stress exposure.

Education and Training
  • BA, Biology, Chemistry, Drury College, Springfield, MO
  • PhD, Anatomy, University of Kansas Medical Center, Kansas City, KS
  • Post Doctoral Fellowship, Neurobiology, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh, Pittsburgh, PA, Pittsburgh, PA

Research

Overview

Stress and pain have an intimate and reciprocal relationship with one another. When experienced acutely, stress can diminish the perception of pain, allowing for sometimes life-saving actions. Conversely, when experienced chronically, stress can increase the perception of pain and exacerbate ongoing symptoms associated with chronic pain states. In particular, stress experienced early in life can have a permanent impact on how pain is perceived and increase overall morbidity. The focus of my laboratory is to understand how stress experienced across the lifespan affects pain processing both in the central nervous system and out in the periphery. We use mouse models of early life stress or insult to study changes within limbic structures, using molecular and imaging technology, that regulate both the stress response system and downstream modulation of incoming pain signals. We use pharmacological and lifestyle interventions, to either improve or exacerbate comorbid outcomes of early life stress, including urogenital hypersensitivity, anhedonic behaviors, and metabolic disorder. Our overall goal is to identify key mechanisms underlying these stress-induced outcomes as a means of identifying potential therapeutic targets for translation into a clinical setting.