Aberrant hippocampal morphology and function in Post-Traumatic Stress Disorder

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dc.contributor.advisorKozicz, Tamas
dc.contributor.advisorHomberg, Judith
dc.contributor.authorMadder, Leonie
dc.date.issued2016-07-25
dc.description.abstractPost-Traumatic Stress Disorder (PTSD) is a debilitating disorder that affects approximately 8% of the population. It can be caused by experiencing a traumatic event and is characterized by symptoms like insomnia, hypervigilance and hyperarousal, and intrusive memories (i.e., flashbacks and nightmares) of the event. Over-generalization of the trauma memory has been suggested to underlie these intrusive memories triggered by indiscriminate environmental factors, and has been related to deficits in hippocampal function. Particularly pattern separation, the process by which memories are stored as unique representations resistant to confusion, mediated by the dentate gyrus (DG), may be compromised. However, since most evidence originates from patient studies that are done retrospectively, it is unknown whether this abnormal hippocampal functioning is in fact part of pathology or constitutes a predisposition to PTSD. Here, we used a validated mouse model for PTSD-induction to induce a PTSD-like phenotype in part of the mice, whereas others are resilient and do not display any PTSD-related symptoms. This model perfectly mimics the human situation, in which only 20 - 25% of the individuals experiencing a trauma will ultimately develop the disorder, whereas the majority stays healthy. We assessed fear generalization, and monitored hippocampal activity (using arterial spin labeling) and the PTSD-associated neuroendocrine changes (i.e., corticosterone levels) over the course of PTSD-development in PTSD-like compared to resilient mice. Moreover, Golgi staining enabled us to assess spine density in the ventral DG as the neurobiological template for pattern separation. In line with literature, PTSD-like animals displayed no fear generalization, but did display suppressed corticosterone response to stress. Moreover, we observed reduced hippocampal activity in PTSD-like mice, but only after trauma induction, indicating the reflection of pathology rather than a predisposition. Lastly, spine density in the ventral DG was significantly reduced in PTSD-like mice. These results indicate that the hippocampal dysfunction associated with PTSD is a consequence of PTSD development, and that high stress-induced corticosterone levels might be protective for the development of PTSD.en_US
dc.embargo.lift2040-07-25
dc.identifier.urihttp://hdl.handle.net/123456789/3529
dc.language.isoenen_US
dc.thesis.facultyFaculteit der Sociale Wetenschappenen_US
dc.thesis.specialisationResearchmaster Cognitive Neuroscienceen_US
dc.thesis.studyprogrammeResearchmaster Cognitive Neuroscienceen_US
dc.thesis.typeResearchmasteren_US
dc.titleAberrant hippocampal morphology and function in Post-Traumatic Stress Disorderen_US
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