Bryson Dabney; Sean Pickard, Brigham Young University
According to the United States Department of Veteran’s Affairs, an average of 11-20% of deployed US soldiers return home with post-traumatic stress disorder (PTSD). In addition to this, 8% of the American population will develop this disorder at some point in their lives (ptsd.ne.gov). Because of these statistics, a cure for PTSD appears at the global forefront of modern research. PTSD induces memories that are aberrantly strong. This enhanced memory is measured physiologically as increased long-term potentiation (LTP), the primary cellular mechanism mediating learning and memory. These enhancements are noted in the hippocampus, the memory center of the brain, along with the amygdala and prefrontal cortex. It is thought that these increases are mediated by increased corticosterone and/or increased norepinephrine that occur by over-activation of sympathetic responses. Therefore, to help treat PTSD, physicians have employed an adrenergic antagonist or glucocorticoid receptor antagonist that can be administered to soldiers before deployment to help decrease the adverse effects of PTSD. Our goal is to examine whether these drugs can be used in a true prophylactic manner to prevent the onset of PTSD. To study this, we set up our research with control rats and stressed rats. We induced PTSD in the stressed rats by using seven consecutive days of social defeat and two weeks of chronic light. Through electrophysiology, we recorded LTP in the ventral prelimbic cortex (PrL) of the pre-frontal cortex, ventral hippocampus and lateral amygdala in both the stressed and control rats. Injections consisting of propranolol and mifepristone were administered to the rats before social defeat and subsequent experimentation. Our data shows that the levels of LTP in the ventral hippocampus were significantly higher for the PTSD rats compared to non-stressed controls and stressed rats with prophylactic injections. We also see a trend of increased LTP in the ventral PrL of the pre-frontal cortex of the PTSD rats. In the lateral amygdala, ventral hippocampus, and the ventral PrL of the pre-frontal cortex, the prophylactic injections were shown to decrease levels of LTP compared to stressed rats that did not receive injections. We have found that the adverse effects of PTSD can be altered with the use of propranolol and mifepristone. These results could prove important as a potential mechanism to prevent PTSD prophylactically for individuals, such as soldiers, who are entering stressful situations.