Cortex moteur | EPFL Graph Search

Le cortex moteur désigne l'ensemble des aires du cortex cérébral qui participent à la planification, au contrôle et à l'exécution des mouvements volontaires des muscles du corps. D'un point de vue anatomique, le cortex moteur est situé dans la partie postérieure du lobe frontal, au niveau de la région caudale de la circonvolution frontale ascendante en avant du sillon central. Le cortex moteur est en interaction constante avec d'autres structures nerveuses impliquées dans le mouvement comme le système des ganglions de la base et le cervelet. Divisions du cortex moteur Le cortex moteur peut être divisées en plusieurs aires fonctionnelles :

le cortex moteur primaire ou aire motrice primaire (noté M1) commande directement l'exécution du mouvement ;
le cortex moteur secondaire (M2) ou cortex pré-moteur inclut : ** le cortex prémoteur latéral ou aire prémotrice situé sur la surface externe du lobe frontal, en avant de M1 qui contrôle l'organisation des mouvements des muscle

Reverse engineering the motor control system

Berat Denizdurduran

Mammalian motor control is implemented by a combination of different networks and system, working coherently to plan the movement of the body or a limb and to execute this movement a dynamical environment. While it is believed that complex, voluntary movements are planned in the motor areas of the cortex, the execution of the movement is controlled by a combination of cortical and cerebellar networks together with central pattern generators and reflex circuits in the spinal cord. In this thesis, we propose an abstract model that captures the basic properties of mammalian motor control, using the example of two different movements: arm movements as well as locomotion. Our model consists of three parts: first a high-level network, that learns movements, using a combination of actor-critic based reinforcement learning and Optimal Control theory. The second part corresponds to spinal reflex circuits that execute basic movements of the musculo-skeletal system. They are modeled by a simple neural network, that learns the dynamic properties of the muscoloskeletal system by the mechanism of spontaneous motor activity (muscle twithing) combined with a Hebbian learning rule. We demonstrate that this network can learn the antagonistic control of joint movements. The final part of the model is a cerebellar network, that translates a complex movement trajectory, such as reaching, and activates the spinal reflex circuits to execute the movement. The mapping between the cerebellar neurons and the spinal reflex circuits are trained with artificial neural networks. Using a musculoskeletal arm model, we demonstrate that the proposed neural motor control model can generate the movement to arbitrary goal position.

EPFL2019

Axonal and Dendritic Morphology of Excitatory Neurons in Layer 2/3 Mouse Barrel Cortex Imaged Through Whole-Brain Two-Photon Tomography and Registered to a Digital Brain Atlas

Sylvain Crochet, Georgios Foustoukos, Yanqi Liu, Carl Petersen

Communication between cortical areas contributes importantly to sensory perception and cognition. On the millisecond time scale, information is signaled from one brain area to another by action potentials propagating across long-range axonal arborizations. Here, we develop and test methodology for imaging and annotating the brain-wide axonal arborizations of individual excitatory layer 2/3 neurons in mouse barrel cortex through single-cell electroporation and two-photon serial section tomography followed by registration to a digital brain atlas. Each neuron had an extensive local axon within the barrel cortex. In addition, individual neurons innervated subsets of secondary somatosensory cortex; primary somatosensory cortex for upper limb, trunk, and lower limb; primary and secondary motor cortex; visual and auditory cortical regions; dorsolateral striatum; and various fiber bundles. In the future, it will be important to assess if the diversity of axonal projections across individual layer 2/3 mouse barrel cortex neurons is accompanied by functional differences in their activity patterns.

FRONTIERS MEDIA SA2022

Axon regeneration and circuit reorganization after complete spinal cord injury

Sabry Leonardo Barlatey

First human trials involving neuroprosthetic rehabilitation demonstrated recently that significant functional benefits can be achieved with lumbosacral neuromodulation and reorganized spared projections. However, complete spinal cord injuries (SCI) wholly isolate infralesional circuits from any supraspinal control, leading to irreversible motor deficits that neuroprosthetics still fails to address. As axons fail to regrow across the lesion site, neuroregenerative research after SCI has been dogmatically focusing attention on minimizing the environmental inhibitions to axon regeneration. In the present work, we demonstrate that spontaneous axon regeneration failure can be reversed, and that propriospinal axons are able to grow across complete non-neural lesion cores when the required facilitators are provided. We identified three mechanisms needed for propriospinal regrowth : i) enhancing neuronal intrinsic growth capacities using viral technologies, ii) remodeling the lesion core with growth factors, in order to densify permissive substrates, and iii) guiding axons chemically across the SCI site. Propriospinal neurons - that coordinate different spinal segments in healthy conditions - are known to support recovery of locomotion in incomplete models of spinal cord injury. However, restoring a robust descending bridge of propriospinal axons does not by itself promote any functional benefit. We hypothesize that a lack of somatosensory feedback to the motor cortex (M1), together with insufficient descending motor control, may prevent coherent exchange of information between lumbosacral and cortical motor centers. Therefore, we explored the neuroregenerative potential of reticulospinal axons - which are projected from the brainstem to the spinal cord - as a second relay for the descending motor cortical command. Together with axon guidance and lesion remodeling, our viral manipulation of intrinsic growth programs induced limited yet significant reticulospinal regeneration into the lesion core. In order to enhance this reticulospinal regrowth, we explored activity-dependent mechanisms of neurite growth control. As we observed that activity does not recruit growth programs after SCI, we revealed a possible divergence between the mechanisms that underly reticulospinal axon regrowth and neurite sprouting. In the mean time, we are developing a somatosensory interface that aims at restoring sensory feedback to the motor cortex after complete SCI. Based on hindlimb electromyographic activity, we linked locomotion to optogenetic neuromodulation of the motor thalamus, and were able to evoke responses in M1 by selectively activating thalamocortical projections, both before and after complete spinal lesion. Such technology enables a direct recruitment of thalamic nuclei that gate motor learning and motor planning at a cortical level. Coming experiments will test wether a strategy combining propriospinal regeneration with locomotion-dependent thalamocortical modulation is sufficient to restore voluntary stepping after complete SCI.

EPFL2019

Axon regeneration and circuit reorganization after complete spinal cord injury

Sabry Leonardo Barlatey

EPFL2019