Etude des mécanismes de plasticité neuronale dans le système visuel adulte blessé in vivo

 

Vincent Pernet

Université Laval

 

Domaine : Neuroscience, santé mentale et toxicomanies

Programme chercheurs-boursiers - Junior 1

Concours 2014-2015

Many ophthalmic diseases such as glaucoma or optic neuritis involve retinal ganglion cell (RGC) degeneration. These neurons are the only ones to possess an axon in the optic nerve through which the visual information travels and is transmitted to cerebral neurons. The death of RGCs or their axon damage in the optic nerve results in irreversible visual deficits. However, a relatively important number of cells are often spared after monocular injury while the opposite eye remains intact. My research work is focused on the mechanisms of plasticity in intact and lesioned adult retinal neurons.

In my research program, I propose to study the inflammatory mechanisms that can promote 1) axonal regeneration in the injured optic nerve and 2) those that can induce the plasticity of spared RGCs, i.e. for which axons are still connected to visual brain regions. These two types of plasticity will be analyzed in experimental models of injury in adult mice. Once identified, molecules required for inflammation-induced neuronal plasticity will be specifically modulated in RGCs by gene therapy. By this manner, RGC plasticity will be controlled without disturbing the function of other retinal cells. The anatomical plasticity will be assessed by tracing axonal trajectories between the eye and the brain with fluorescent molecules, in three-dimensions. At the functional level, visual recovery will be monitored by using a non-invasive behavior test in freely moving mice.

The complete regeneration of severed axons to the brain could restore visual perception whereas manipulating spared RGC plasticity could compensate for the loss of some retinal neurons after a partial monocular lesion such as retinal ischemia.