Erin Saito; Gabriel Melendez; Roxanne Miller, Brigham Young University
Fear-based experiences, such as those related to PTSD, have been shown to induce changes within regions of the brain involved in emotion and memory processing (hippocampus, amygdala, prefrontal cortex). However, because the mechanisms governing PTSD are not fully known, an effective protocol for inducing PTSD-like symptoms becomes necessary for accurately studying its mechanisms. We compared the effectiveness of two models of stress induction in rats - two days of single prolonged stress (SPS) with two weeks of chronic light, versus social defeat with two weeks of chronic light. SPS consisted of two hours of restraint, followed by 20 minutes of forced swim and loss of consciousness via isoflurane gas, twice over two weeks. Social defeat consisted of seven consecutive days of “beating” by an older, more aggressive rat for five minutes, followed by 25 minutes of “isolation” from the larger rat by a mesh divider. We used elevated plus maze and light-dark transition assays to test for anxiety-like and depression-like behaviors, and recorded fEPSPs (field excitatory post-synaptic potentials) from CA1 of the ventral hippocampus to detect differences in synaptic plasticity, specifically long term potentiation (LTP), to determine which model of stress was more effective in inducing PTSD-like changes. In the elevated plus maze and light-dark transition assays, both models significantly increased anxiety and depression-like behaviors compared to controls. However, because the social defeat model caused greater anxiety-like behavior than the SPS model in the behavioral assays, and significantly increased LTP at the ventral hippocampus, we concluded that the social defeat with chronic light model was more effective in inducing both PTSD-like behavioral and physiological changes.