Corentin Le Magueresse
  • E-mail :[email]
  • Phone : +33 1 45 87 61 47
  • Location : Paris, France
Last update 2019-05-07 17:35:33.21

Corentin Le Magueresse PhD Neuropharmacology

Course and current status

2013-present: tenured INSERM investigator

Institut du Fer à Moulin (INSERM & Sorbonne Université), Paris

www.ifm-institute.fr/en/

2006-2013: postdoctoral scientist

University of Heidelberg and German Cancer Research Center (Monyer lab)

2001-2006: PhD student

Institut Pasteur, Paris (Changeux lab) and International School for Advanced Studies, Trieste (Cherubini lab)

Scientific summary

Since the beginning of my scientific career I have been interested in mechanisms sculpting neural circuits during postnatal development. While the basic layout of the brain is first established by genetic programs and intrinsic activity, the developing brain rapidly becomes remarkably plastic, capable of remodeling synaptic connections in response to changing experiences. This experience-dependent sculpting of neuronal circuits peaks during specific time windows called critical periods.

I am currently interested in two forms of critical period plasticity:

1)    During postnatal development, the brain generates an excess of synapses. The inactive fraction of these synapses is eliminated in adolescence, a phenomenon known as synaptic pruning. Synaptic pruning defects have been identified in some brain disorders, particularly schizophrenia. Recent research shows that genes of the complement, a system contributing to innate immunity, mediate synaptic pruning in the brain. Complement genes are also associated with schizophrenia. We investigate the role of distinct complement components in network remodeling and microglia-neuron interactions in the adolescent brain using novel transgenic mouse models, optogenetics, electrophysiology, histology, imaging, and behavioral studies.

2)    A critical period has been well characterized in the visual cortex where permanent changes in neuronal networks take place following transient closure of one eye in young but not in adult mammals. Converging evidence implicates glutamatergic inputs onto parvalbumin-expressing interneurons in the onset of this critical period for visual cortex plasticity. However, the underlying molecular and synaptic mechanisms remain unclear. Using a multidisciplinary approach including novel transgenic mice, viral vectors, and electrophysiology, we study the contribution of specific synaptic proteins to network plasticity during the critical period in visual cortex.

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