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Session XVII : Cell <strong>signaling</strong> in health <strong>and</strong> disease Poster XVII, 12<br />

Are key factors of signalling intracellular pathways involved in the regulation of<br />

neuromuscular changes after disuse conditions ?<br />

Erwan Dupont, Marie-Hélène Canu, Maurice Falempin, Yvonne Mounier <strong>and</strong> Laurence<br />

Stevens<br />

Laboratoire de Plasticité Neuromusculaire, EA 1032, IFR 118, Unité de Neurosciences et<br />

Physiologie Adaptatives, Bât SN4, Université des Sciences et Technologies de Lille,<br />

59655 Villeneuve d’Ascq cedex, France<br />

The performance of the neuromuscular system is highly dependent on activity. A situation of<br />

disuse induced by hypodynamia-hypokinesia (HH) in rats induces profound changes in<br />

skeletal muscles like phenotype transformations, <strong>and</strong> a marked atrophy resulting from a loss<br />

in mass <strong>and</strong> protein content. HH is also a model of hindpaw sensory deprivation since in these<br />

conditions, the cutaneous receptors located on the foot sole are deactivated. HH produces a<br />

cortical reorganisation of the somatosensory cortex (SmI), indicating the existence of a<br />

neuronal plasticity.<br />

The factors responsible for these impairments are still unknown <strong>and</strong> the cellular <strong>and</strong><br />

molecular processes sustaining this “plasticity” are not well described. The major aims here<br />

were to better underst<strong>and</strong> the mechanisms i) that characterized muscular plasticity,<br />

phenotypical transitions <strong>and</strong> atrophy, <strong>and</strong> ii) involved in cortical plasticity (sensory<br />

conduction <strong>and</strong>/or cortical excitability changes, regulation of neurotransmitter <strong>and</strong><br />

neurotrophin expression). Among multiple intracellular signalling pathways, one major is<br />

implied in controlling more specifically muscle <strong>and</strong>/or nervous plasticity : the MAPKinase<br />

(Mitogen-Activated Protein Kinase) cascade. We induced modulations of transformations<br />

using different periods of disuse (from 7 to 28 days of HH) in rats. Key markers of<br />

MAPKinase cascade were followed : ERK, JNK <strong>and</strong> p38. Their protein expressions were<br />

evaluated by western blots (using specific antibodies) performed on all the animal groups, as<br />

well at the muscular as at the cortical levels. For the muscles, the expression of all MAPK<br />

markers was increased in a time-dependent manner of disuse, excepted for 14 days of HH, the<br />

increase being lower than for 7 <strong>and</strong> 28 days. At the cortical level, the increase was less<br />

pronounced <strong>and</strong> not disuse-dependent.<br />

Taken together, these results may help to develop strategies that aim at attenuating the effects<br />

of pathologies, like long-term immobilizations, on the neuromuscular system.<br />

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