13 research outputs found

    Etude électrophysiologique préliminaire de la régénération du nerf alvéolaire inférieur

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    Un protocole expérimental a été mené sur 8 lapins afin d’évaluer la régénération du nerf alvéolaire inférieur (IAN) 6 mois après section complète et suture conventionnelle. Le risque de lésions nerveuses pouvant survenir à la suite de certains actes de chirurgie buccale, comme les extractions de dents de sagesse mandibulaires, reste trop souvent méconnu. Pourtant dans 0,05 % des cas, il existe à une lésion irréversible qui pourrait justifier une microsuture nerveuse. Dans cette étude, des tests électrophysiologiques ont été réalisés à J + 180 pour quantifier de façon objective la régénération du nerf. Une étude histologique a permis de comparer structurellement mais aussi quantitativement les fibres nerveuses saines et celles remaniées. Les résultats obtenus montrent une régénération fonctionnelle dans 7 cas traités. (Med Buccale Chir Buccale 2003; 9: 21-27

    Dendritic spine remodeling induced by hindlimb unloading in adult rat sensorimotor cortex.

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    A sensorimotor restriction, for instance in patients confined to bed, induces an impairment in motor function, which could be due to structural and functional reorganization of the sensorimotor cortex. Hindlimb unloading (HU) is a rodent model used to reproduce the chronic weightless bearing and reduction in hindlimb movement. In this study, we determined whether a 14-day period of HU in adult rats leads to dendritic spine plasticity. For this purpose, we visualized a large number of spines on pyramidal neurons located in superficial and deep layers of the cortex within the hindpaw representation area, by means of confocal microscopy. Spines were classified according to their shape, as stubby, thin, mushroom, or filopodium. Spine density was increased (+26%) after HU. The increase concerned mainly filopodium spines (+82%) and mushrooms (+33%), whereas no change was noticed for stubby and thin spines. Spine length was decreased, whatever their shape. Head diameter evolved differently depending on the layer: it was increased in superficial layers and decreased in deeper ones. These results indicate that morphological changes accompany functional reorganization of motor cortex in response to a decrease in sensorimotor function during adulthood

    Activity-dependent changes in the electrophysiological properties of regular spiking neurons in the sensorimotor cortex of the rat in vitro.

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    International audienceSensorimotor performance is highly dependent on the level of physical activity. For instance, a period of disuse induces an impairment of motor performance, which is the result of combined muscular, spinal and supraspinal mechanisms. Concerning this latter origin, our hypothesis was that intrinsic properties and input/output coupling of cells within the sensorimotor cortex might participate to the alteration in cortical motor control. The aim of the present study was thus to examine the basic electrophysiological characteristics of cortical cells in control rats and in animals submitted to 14 days of hindlimb unloading, a model of sensorimotor deprivation. Intracellular recordings were obtained in vitro from coronal slices from cortical hindpaw representation area. We have also made an attempt to determine the morphological characteristics as well as the location of the investigated neurons by biocytin labelling. Passive properties of neurons were affected by hindlimb unloading: input resistance and time constant were decreased (-20%), the rheobase was increased (+34%), whereas the resting potential was unchanged. The frequency-current relationships were also modified, the curve being shifted towards right. The size of body area of recorded neurons was unchanged in unloaded rats. Taken together, these data reflect a decrease in excitability of cortical cells in response to a decreased cortical activation

    P53 inactivation leads to impaired motor synchronization in mice.

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    We have combined genetic and pharmacological approaches to investigate the behavioural consequences of inactivation of the murine p53 protein. Our behavioural analysis revealed that p53-null mice (p53KO) exhibit a very specific and significant motor deficit in rapid walking synchronization. This deficit, observed using the rotarod test, was the only behavioural defect of p53KO mice. We demonstrated that it was not due to an increase in neuronal number or abnormal connectivity in the olivo-cerebellar system, thought to control motor synchronization. In order to test the role of p53 in the central nervous system, we injected a pharmacological inhibitor of p53 activation, pifithrin-alpha, into the cerebellum of wild-type mice. This treatment mimicked the walking synchronization deficit of p53KO mice, suggesting that presence of p53 protein in the cerebellum is necessary to execute this synchronization of walking. Our investigation reveals a functional role of cerebellar p53 protein in adult walking synchronizatio
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