Team members


Cellular Interactions, Neurodegeneration and Neuroplasticity

We investigate the organization and functional dynamics of brain neuronal circuits, their adaptive capacities and the mechanisms underlying their pathological dysfunction and neurodegeneration, with focus onto the basal ganglia network.

Our main research interest is on synaptic transmission, neurodegeneration and neuroplasticity in the adult brain. Communication between neurons at the level of their connections, called synapses, is the substrate of information processing in the networks underlying brain functions. Synaptic transmission is a highly dynamic and regulated process, influenced by glial cells, whose abnormalities are associated with a number of brain diseases (concept of synaptopathies). Neurodegeneration is a pathological process that triggers progressive dysfunction and death of nerve cells. Understanding the pathological mechanisms triggering and sustaining neurodegeneration (pathogenesis), its consequences on  circuit function and the mechanisms that help neurons to manage cellular stress is essential for the development of curative or disease-modifying treatments for devastating neurodegenerative disorders, such as Parkinson’s disease (PD). Neuroplasticity refers to the capacity of the nervous system to adapt in response to experience and to internal or external stimulations by modifying the interactions between nerve cells, including changes in the number of synapses and the efficacy/strength of synaptic transmission (synaptic plasticity), or by generating new nerve cells. This faculty is not limited to development, but occurs lifelong, although declining with aging. Neuroplasticity has been notably involved in learning and memory processes. It also occurs under pathological conditions or in response to chronic treatments. Such adaptive changes can represent compensatory mechanisms counteracting the deficits triggered by neuronal dysfunction or death, delaying the symptom onset, or, on the contrary, can participate in or even aggravate the deficits.

The team is investigating these processes in the context of basal ganglia (BG)-related functions and pathologies, in particular PD, a movement disorder characterized by the degeneration of midbrain dopamine neurons innervating the striatum, the main BG input station. Through collaborations, our work also addresses fundamental and clinically-relevant issues in the context of other neuropathologies, including autism spectrum disorder (ASD), Alzheimer’s disease and Charcot-Marie-Tooth disease.

Golgi staining-like view of a striatal medium-sized spiny neuron obtained by viral retrograde tracing, which reveals its thin dendritic arborizations and high density of spines that are primary post-synaptic seats of excitatory connections.


Our last publications


of the teams

Team members

They drive our research


They contributed to our research
Maxime Assous
Research Associate, Center for Molecular and Behavioral Neuroscience, Rutger University, Newark, NJ, USA
Abid Oueslati
Associate Professor (Department of Molecular Medicine, Laval University), Director of the Molecular and Cellular Neurodegeneration Laboratory, CHU Research Center, Quebec City, Canada

Funding bodies

They support our research
Fondation Alzheimer
Fondation de France