Organisation du circuit locomoteur du mésencéphale et réorganisation après lésion de la moëlle épinière
|Abstract:||Spinal cord injuries cause a functional motor deficit of varying importance depending on their location and their severity. After incomplete spinal cord injury, it is possible to notice in animal models and patients a certain functional recovery occurring on a period going from a few weeks to several years. This recovery may occur thanks to an anatomical reorganization of the spinal locomotor circuit and supraspinal locomotor centers. Among these centers is the mesencephalic locomotor region (MLR) which is a functional region able to initiate and modulate locomotion. Its exact anatomical correlates are still a matter of debate but they could include the cuneiform nucleus (CnF), a cluster of glutamatergic neurons, the pedunculopontine nucleus (PPN) that is cholinergic and glutamatergic, the deep mesencephalic nucleus (MRN/DpMe) that is glutamatergic and the laterodorsal tegmentum which is formed by neuronal populations similar to the PPN. Some studies suggest that there is an increase of projections from the MLR to the brainstem after lesion and that the glutamatergic neurons of the CnF can initiate and accelerate locomotion. Using retrograde tracing, stereological analysis and kinematic, we show, in the CnF but also in the contralesional PPN and LDT, that there is a recruitment of MLR glutamatergic projections to the medullar reticular formation. Considering the major role of glutamatergic neurones in locomotion, this recruitment could contribute to motor functional recovery after incomplete spinal cord injury. An anterograde tracing experiment could then help us to confirm that these “new” projections form synaptic connections in the medullar reticular formation and, maybe, in the spinal cord. This project could contribute to specify the optimal deep brain stimulation sites in the MLR to treat motor deficits caused by incomplete spinal cord injuries and maybe also by other pathologies such as Parkinson’s disease.|
|Document Type:||Mémoire de maîtrise|
|Open Access Date:||21 December 2018|
|Collection:||Thèses et mémoires|
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