Abstract
Posttraumatic stress disorder (PTSD) is characterized by exaggerated trauma-related memories, increased avoidance of trauma-related cues and hyperarousal. We employed our recently established mouse model of PTSD in order to characterize the brain matrix which underlies long-term maintenance of those PTSD-likes symptoms. To this end we measured Cytochrome C-oxidase activity (which serves as a marker for lasting changes in cellular metabolism) 2 days or 28 days after exposure to a brief inescapable foot shock. We observed a delayed and rather selective increase in metabolic activity, among others, throughout the hippocampus formation, the prelimbic cortex, the basolateral amygdala and the nucleus accumbens. Cross-correlation analyses revealed distinct patterns of brain activity which are ought to underlie the PTSD-like symptoms. Importantly, amelioration of these symptoms by chronic fluoxetine treatment was accompanied by changes in the activity patterns. Taken together our data demonstrate that the maintenance of PTSD-like symptoms is associated with a long-lasting increase in metabolic activity of distinct brain structures. Moreover, activity patterns appeared to be symptom-specific. Experiments in progress investigate whether disruption of such activity patterns by deep-brain stimulation may ameliorate the severity of PTSD-like symptoms.
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