Research Group
Silva Group
Circuits Neuroscience Lab
Our lab aims at understanding how the brain processes emotions, how intense emotional experiences are encoded into memories and how these memories can be subsequently updated. In particular, we focus on fear and investigate new avenues to attenuate intense emotional memories following traumas, with the final goal of developing better treatments for fear-related disorders, such as PTSD and phobias.
The challenge
How do animals integrate new information to update previously encoded memories? What happens when this process is impaired? The capacity to adapt to a dynamic environment is a fundamental ability for survival. For this, animals need to constantly integrate new information, update their representation of the world and adjust their behavior accordingly. A fundamental aspect of this process is the capacity to update previously encoded memories. My lab aims at understanding how the fine balance between memory stability and memory flexibility is achieved and what happens when this balance is impaired.
Main research areas
Thalamic circuits of fear extinction
The nucleus reuniens of the thalamus acts as a central hub for extinction of remote fear memories. Here, we combine, projection-specific transcriptomics, whole-brain input-output tracing (TRIO + iDISCO), and ex vivo electrophysiology to unravel the neurobiological mechanisms at the basis of such newly discovered thalamic function in healthy subjects as well as PTSD models in the mouse.
Effect of chronic pain on thalamic extinction circuits
In light of the high comorbidity between PTSD and chronic pain, as well as the documented impairments in fear extinction capacity in pain conditions, we are investigating the interactions between pain-modulating circuits and the thalamic-centered fear extinction network.
Prenatal stress as a risk factor for Alzheimer’s disease
Using the APPswe(K670M/N671L), PSEN1dE9 mouse line (APP/PS1) as a model for Alzheimer’s disease, we have shown that gestational stress induces an acceleration of Aß pathology in the aged offspring. This is accompanied by increased inflamation as well as increased neuronal excitability in the stressed embryos, while in the adult brain prenatal stress is associated with increased baseline activity but decreased networks functional connectivity. We are now investigating the link between such altered immunological signalling and the associated neuronal disfunction.
Group members
