Introduction

Memory and emotions are intrinsically linked: memories associated with strong emotions such as fear or pleasure are better and more vividly remembered. This constitutes a clear adaptive advantage to avoid future threats and seek rewards. However, such memory function can become maladaptive following traumatic experience, when neutral contexts trigger the vivid recall of traumatic memories, such as in post-traumatic stress disorder (PTSD). Two of the primary brain structures involved in emotional memories are the hippocampus and the amygdala. Canonically, it is thought that the hippocampus processes context, while the amygdala processes emotional valence. Indeed, both the amygdala and the hippocampus are required to establish associations between a threat and physical location (place-threat associations), such as in contextual fear conditioning. However, surprisingly little is known about the in vivo physiology of interactions between the hippocampus and the amygdala. Notably, amygdala-hippocampus interactions have rarely been studied during sleep, despite the well-known role of sleep in memory consolidation (i.e. the gradual reinforcement of memories over time), and emotional regulation. 

Projects

In my team, we are studying neural activity in the hippocampus and amygdala during REM and Non-REM sleep, the two major stages of sleep. These sleep stages are associated with canonical hippocampal oscillations that are believed to play a role in brain-wide communication, and in hippocampus-amygdala interactions in particular. During Non-REM sleep, the hippocampus displays fast oscillations called “ripples”, that are crucial for spatial memory consolidation. On the other hand, theta oscillations (8hz) are typical of REM-sleep. Using a combination of closed-loop optogenetic manipulations and correlation analysis of large scale neuronal ensembles recorded in the hippocampus and amygdala of freely sleeping rats after aversive learning, we want to understand how sleep oscillations can coordinate neural activity through the hippocampus-amygdala network to sustain the consolidation of aversive memories. This knowledge will help us understand how these sleep-dependent consolidation processes are affected in PTSD, which we study in parallel in rodent models of the disease.

Impact

PTSD and generalized anxiety constitute a rising concern for global public health, together with a global decrease in the quality and quantity of sleep. It is thus crucial to understand the fine mechanisms sustaining the role of sleep in emotional processing at large (memory, emotional regulation) in normal conditions, and in pathological conditions. For example, new therapeutic approaches to PTSD include sleep-deprivation after a trauma. Basic research must parallels these developments in medicine to be able to refine therapeutic targets. My team’s projects will deepen our knowledge of the precise neurophysiological mechanisms potentially affected in human patients. On the long term, it will thus allow for the development and implementation of accurate prevention and curing strategies focused on sleep in anxiety disorders.