Détails de la réservation
- Le : 14 September 2018
- De : 10 h 30
- à : 12 h 30
- Salle : Amphi Centre Broca Nouvelle - Aquitaine
Détails de l'évènement
Marloes Henckens
Dr. Marloes Henckens, Department of Cognitive Neuroscience,
Donders Institute for Brain, Cognition and Behaviour, Radboudumc Nijmegen, the Netherlands
"The neural signature of trauma susceptibility"
Résumé
Posttraumatic stress disorder (PTSD) is a psychiatric disorder which can develop after exposure to a traumatic event. Flashbacks, spontaneous recollection and recurrent nightmares of the trauma are amongst the most devastating symptoms of PTSD, through which patients continuously relive their trauma. Interestingly, only a small fraction (8-10%) of all trauma-exposed individuals eventually develops PTSD, whereas the rest is resilient and remains healthy. But how is the vulnerable brain different from the resilient one and when do these differences arise? Understanding the mechanisms behind these inter-individual differences could contribute to new clinical intervention strategies.
The use of a mouse model for PTSD allows us to study the mechanisms underlying relative resilience or susceptibility to PTSD in a longitudinal fashion, under controlled settings, while allowing for more invasive brain measurements. In this model, mice are first exposed to a traumatic event (i.e., severe unpredictable foot shock), followed by a trigger (i.e., mild predictable foot shock) in a different context one day later. Following a week of recovery, eventual development of PTSD-like symptomatology is assessed using a battery of behavioural tests to identify mice resilient and vulnerable to the trauma.
Combining this model with functional MRI obtained both before and after trauma exposure, allowed us to study the development of a potential imbalance in neural network function as a consequence of trauma in the PTSD-vulnerable vs resilient brain, as well as the potential presence of neural abnormalities prior to trauma exposure in these animals. To study brain responses to the trauma itself, we used the so-called targeted recombination in active populations (TRAP) mice, in which the injection of tamoxifen opens up a temporal window in which all neurons expressing certain immediate early genes (reflecting neuronal activity), are permanently fluorescently labelled. We injected these animals with tamoxifen just prior to trauma exposure, and again assessed PTSD-symptoms later on. By re-exposing them to the traumatic context just before sacrifice and analysing trauma retrieval-induced neuronal activity by immunohistochemistry, we were moreover able to analyse the storage of the trauma memory into long-term memory.
This allowed us to assess whether aberrant storage of the trauma memory could explain the emotional hypermnesia and contextual hypomnesia of the trauma that seem to characterize PTSD patients.
Invitant : Aline Desmedt, PhD , Maitre de Conférence au Neurocentre Magendie, Team 'Pathophysiology of declarative memory
Responsable
- Nom : Desmedt Aline