Decreased expression of synaptic proteins in a mouse model of posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) is a common and debilitating psychiatric disease. Although hippocampal atrophy and several other factors have already been found to be associated with PTSD, the pathomechanisms underlying this anxiety disorder still remain elusive. Clinical fMRI studies and the fact that the hippocampus is a known player in fear extinction processes fuelled the assumption that alterations of hippocampal function most likely play a central role in PTSD pathogenesis. Aiming at identifying pathomechanisms and potential PTSD biomarkers, we compared the expression levels of several synaptic, glial and stress-associated proteins in hippocampal tissue of either traumatized or unstressed control mice. In traumatized mice, we found a decreased protein expression of hippocampal synaptic vesicle proteins while neuronal marker proteins remained unchanged, indicating a synapse specific effect and excluding the possibility of an overall reduction of neuronal cell number. Reduced expression of synaptic vesicle proteins in posttraumatic stress disorder could implicate impaired synaptic transmission either by depletion of neurotransmitter due to reduced vesicle number or by synapse retraction.