Anxiety disorders include four major classes of psychiatric diseases (DSM-5) and represent the most prevalent psychiatric conditions, with an estimated prevalence of 18% among adults, and more than 28% over a lifetime. Despite the high personal and societal costs of anxiety disorders, few therapeutic targets have been identified for the treatment of anxiety, and available treatments have limitations.
A leading hypothesis posits that anxiety disorders are caused by dysfunctions of the neural circuits controlling the level of anxiety or emotional valence in healthy conditions. However this hypothesis remains untested, and the brain circuit dysfunctions present in anxiety disorders remain unknown. Human imaging has identified that the activity of the insular cortex (insula) is altered in patients with anxiety disorders.
Our research program aims at identifying cellular, synaptic and molecular alterations of circuits of the insular cortex in animal models of anxiety disorders. We also envision to develop strategies to restore those dysfunctions, with the long term goal to translate our fundamental findings to clinical trials.
More informationOur research is funded by the Région Nouvelle Aquitaine (Neurocampus Project), the Excellence initiative of the University of Bordeaux and the ATIP-Avenir Program of CNRS and INSERM.
Responses of the insular cortex (IC) and amygdala to stimuli of positive and negative valence are altered in patients with anxiety disorders. However, neural coding of both anxiety and valence by IC neurons […]