A mouse study has revealed the brain becomes overly stimulated after a traumatic event causes an ongoing, frenzied interaction between two brain proteins long after they should have disengaged. However, the injection of newly developed drugs into the hippocampus within a five hour window calmed this process, and prevented the development of a post-traumatic fear response.
The new research shows the potential for PTSD occurs when a stressful event causes a flood of glutamate, which then interacts with a second protein (Homer1a). This protein continues to stimulate metabotropic glutamate receptor 5 [mGluR5] after the glutamate has dissipated. The new drugs bind mGluR5 and reverse its activity.