Miller, Roxanne; Winzenried, Eric; Everett, Anna; Edwards, Jeffrey (Brigham Young University)
Faculty Advisor: Edwards, Jeffrey (Life Sciences, Physiology and Developmental Biology)
Post-traumatic stress disorder (PTSD) is a complex anxiety/depression disorder that affects about 1 out of 4 individuals after a stressful/traumatic experience. One common model to induce PTSD is social defeat (SD) combined with chronic light exposure in rats. First, more naturally anxious rats were selected based on results of an open field test where cat fur and fox urine were placed in one quadrant. Rats were classified as anxious if they avoided that quadrant, froze for long periods of time, did not rear, and frequently urinated or defecated. The naturally anxious rats were used in the SD protocol. Next, the elevated plus maze (EPM) and light-dark transition (LDT) tests were used to detect anxious behavior at the conclusion of SD. The SD protocol caused significant anxious behavior when compared to controls. Next, we performed LTP field electrophysiology experiments in brain slices of ventral hippocampus and basolateral amygdala, regions known to have altered plasticity in PTSD. SD caused a significant increase in long-term potentiation (LTP) in the ventral hippocampus and basolateral amygdala. To determine whether a prophylactic treatment could prevent the physiological changes of PTSD, propranolol and mifepristone were simultaneously administered at 10 mg/kg doses by intraperitoneal (IP) injection one week prior and during the entire duration of SD. These drugs significantly decreased LTP in the VH and BLA back to near-control levels while SD rats with vehicle injections still had elevated LTP.