J-Olivier COQ - Institut de Neuroscience de la Timone (INT).
A 14H, en Salle des thèses (A104), Faculté des Sciences du Sport, Campus de Luminy, Marseille.
Cerebral palsy (CP) is a complex syndrome of various sensory, motor and cognitive disorders, and a main cause of physical disabilities in children. CP appears primarily related to an injury to immature brain and/or abnormal development of brain organization and function ; however, the emergence of motor disorders remains a matter of debate. Abnormal spontaneous movements are usually observed in infants and children who develop CP later. Developmental coordination disorder (DCD or dyspraxia) corresponds to difficulties with or impairments of the organization, planning and execution of movements that begins in the early developmental period rather than be acquired through brain damage. To gain new insights into the underlying mechanisms of developmental movement disorders, we investigated the enduring impact of early abnormal sensorimotor experience (EASE) on gait and posture, musculoskeletal histopathologies, muscle function and morphology, and anatomical and functional organization of the lumbar spinal cord, primary somatosensory (S1) and motor (M1) cortices in adult rats. We show that EASE degrades locomotion, musculoskeletal tissues, the S1 topographical organization and alters neuronal response properties in S1 and M1. However, we find no changes in S1 and M1 neuroanatomy, yet increased glutamate excitability within the hind limb S1-M1 area. Concomitantly, we find high levels of spasticity and hyperexcitability of the lumbar spinal network that match cortical increased excitability. The changes in muscle function and organization appear to correlate spinal cord plasticity, suggesting neuromuscular interplay. In the absence of perinatal brain damage, we show that abnormal patterns of motor outputs and sensory inputs to the immature spinal cord and cortex play a pivotal role in shaping movement abilities and brain functioning through maladaptive, experience-dependent plasticity, as observed in several pathologies.
Dr J-O Coq is a full-researcher at the CNRS (french National Center of Scientific Research) and PI in the Institute of Neuroscience de la Timone (INT) in Marseille, France. He did his postdoctoral trainings in Pr Jon Kaas’ lab at Vanderbilt University (Nashville, TN) and Pr Mike Merzenich’s lab at UC San Francisco ; both of them are members of the US Academy of Science. His current interests are directed toward both sensorimotor plasticity from brain to spinal cord and animal models of human pathologies, such as cerebral palsy and encephalopathy of prematurity. In his team, they developed several rodent models based on either prenatal ischemia, neonatal hypoxia-ischemia or early abnormal sensorimotor experience. They currently use in vivo and in vitro electrophysiological techniques, as well as molecular biology and behavioral experimentation. They also focus on translational research based on such animal models of pathologies.