Synapse in cognition
Synapse et Cognition

IINS

Dans de nombreux cas, le déficit intellectuel, encore appelé retard mental, résulte de mutations génétiques. Chez des souris portant de telles mutations, des déficits d’apprentissage et de neurotransmission sont observés. Notre défi est de cibler les synapses affectées participant aux déficits cognitifs. Nos études suggèrent que l’inefficacité synaptique des projections entre l’hippocampe et l’amygdale serait responsable de l’altération de la mémoire de peur conditionnée. Dans ce contexte, ce déficit mnésique ne serait pas du à un défaut d’apprentissage ou de stockage de nouveaux souvenirs mais à l’incapacité à les restituer. Une compréhension fine des mécanismes pathophysiologiques impliqués dans le déficit intellectuel, nous permettra d’apporter un nouvel éclairage sur cette maladie.


English version

Synapses are plastic. They change their efficacy depending on various parameters, including the respective activities of pre- and post-synaptic neurons. Numerous in vitro studies explored the plasticity repertoire of numerous synaptic populations in the mouse brain, but more rarely with regards to their endogenous inducers. It is no doubt that synaptic plasticity is associated and mediates learning and memory, thus our goal is to identify the neuronal activities that are associated with the learning and execution of cognitive abilities, and to understand how, when and where synaptic plasticity is generated. We are developing cooperative in vivo and in vitro strategies to study the link between synapse and cognition. These include behavioral tests, in vivo pharmacology and optogenetic, and in vitro electrophysiological recording in various brain regions of identified synaptic populations. Future projects will focus on various aspects of spatial learning, and will more and more includes in vivo electrophysiological recordings in freely behaving mice. Ex. Our main objective is to understand the link between synapse and cognition at the synaptic and circuit level. Our recent results show that several mental retardation (MR) mouse models exhibit functional synaptic deficits at cortical projections to the lateral amygdala (LA), a structure involved in the coding of fear memory. We will examine the role of MR proteins in the process of memory formation by analysing biochemical, morphological and physiological changes of cortico-LA synapses in mice submitted to fear conditioning.

Innovative techniques: In vivo electrophysiology, in vivo two-photon imaging of neuronal activity, fluorescence-activated sorting of synaptosomes



Selected publications