Aline Desmedt, Aline Marighetto, P-V Piazza dans Biol Psy

Le 1er septembre 2015

Abnormal Fear Memory as a Model for Posttraumatic Stress Disorder
Aline Desmedt, Aline Marighetto, and Pier-Vincenzo Piazza
Biological Psychiatry September 1, 2015; 78:290–297

Aline Desmedt est dans l’ équipe ‘Physiopathologie de la mémoire déclarative’ d’Aline Marighetto au Neurocentre Magendie dirigé par Pier Vincenzo Piazza.

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Aline Desmedt : Alors que la plupart des modèles animaux actuels de mémoire traumatique se focalisent sur l’hypermnésie liée au trauma, cette revue soutient la thèse selon laquelle l’amnésie vis-à-vis du contexte environnemental du trauma est au cœur de l’état de stress post-traumatique (ESPT). Un modèle de mémoire de type ESPT récemment mis au point chez la souris y est décrit : il fournit le moyen de distinguer une mémoire normale et adaptative d’un épisode de stress d’une mémoire traumatique pathologique, incluant, elle, une telle amnésie. Cette distinction est mise en exergue dans la mesure où elle s’avère cruciale pour l’identification de biomarqueurs de l’ESPT, lesquels diffèrent nécessairement des altérations biologiques adaptatives induites par un stress. »

Abstract PubMed

For over a century, clinicians have consistently described the paradoxical co-existence in posttraumatic stress disorder (PTSD) of sensory intrusive hypermnesia and declarative amnesia for the same traumatic event. Although this amnesia is considered as a critical etiological factor of the development and/or persistence of PTSD, most current animal models in basic neuroscience have focused exclusively on the hypermnesia, i.e., the persistence of a strong fear memory, neglecting the qualitative alteration of fear memory. The latest is characterized by an underrepresentation of the trauma in the context-based declarative memory system in favor of its overrepresentation in a cue-based sensory/emotional memory system. Combining psychological and neurobiological data as well as theoretical hypotheses, this review supports the idea that contextual amnesia is at the core of PTSD and its persistence and that altered hippocampal-amygdalar interaction may contribute to such pathologic memory. In a first attempt to unveil the neurobiological alterations underlying PTSD-related hypermnesia/amnesia, we describe a recent animal model mimicking in mice some critical aspects of such abnormal fear memory. Finally, this line of argument emphasizes the pressing need for a systematic comparison between normal/adaptive versus abnormal/maladaptive fear memory to identify biomarkers of PTSD while distinguishing them from general stress-related, potentially adaptive, neurobiological alterations.