Matthew Bruner

Mentor: Dr. Jennifer Bizon
College of Medicine
"My interests in neuroscience research stems from when I was a senior in high school, where I got a first-look at how the brain functions from my AP Psych course. With an initial fascination of all the intricacies of a neuron, I grew curious as to how something so small operates and provides a means to the brain's cognitive processes. Therefore, I delved into an undergraduate biochemistry degree to begin to understand the inner-workings of a neuron. The knowledge that I accrued from my biochemistry courses fueled my desire to enter a lab and uncover answers to scientific questions firsthand."





Research Interests

  • Molecular Neuroscience
  • Stress/ Aging
  • Cognition/ Behavior

Academic Awards

  • Bright Futures Scholarship (2012-present)
  • Dean's List (2012-2015)
  • University Scholars (2015-2016)


  • National Society of Collegiate Scholars
  • North Central Florida Society for Neuroscience Chapter


  • Brain Awareness Week
  • TOPSoccer
  • Shriner's Camp Care-a-lot

Hobbies and Interests

  • Golf
  • Exercise

Research Description

Alterations of the mPFC Induced by Chronic Variable Stress
Glucocorticoid output from the hypothalamic-pituitary-adrenal (HPA) axis requires regulatory mechanisms to curtail its stress response and regain homeostasis. The medial prefrontal cortex (mPFC) contains glucocorticoid receptors that serve as a negative feedback loop to the HPA axis, but prior studies show that overexposure of glucocorticoids to the mPFC can provoke structural changes and reduce neuronal activity. Little evidence is currently available to pinpoint the molecular alterations causing the depletion of neuronal activity within the mPFC. In this study, young adult (6 months) rats were exposed to a 14-day chronic variable stress paradigm (an unpredictable schedule of stressors including insulin-induced hypoglycemia, 60 min restraint, 7 min swim in 16°C water, predator urine). Western blot analysis on mPFC tissue was used to locate specific alterations of protein expression (i.e. glutamate and GABA receptor subunits).