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Accueil Tous les numéros Volume 33 / Numéro 6-7 (Juin-Juillet 2017) Med Sci (Paris), 33 6-7 (2017) 629-636 Références
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Numéro
Med Sci (Paris)
Volume 33, Numéro 6-7, Juin-Juillet 2017
Page(s) 629 - 636
Section M/S Revues
DOI https://doi.org/10.1051/medsci/20173306020
Publié en ligne 19 juillet 2017
  1. Biering-Sorensen F, Nielsen JB, Klinge K. Spasticity-assessment : a review. Spinal Cord 2006 ; 44 : 708–722. [CrossRef] [PubMed] [Google Scholar]
  2. Sommerfeld DK, Eek EU, Svensson AK, et al. Spasticity after stroke : its occurrence and association with motor impairments and activity limitations. Stroke 2004 ; 35 : 134–139. [CrossRef] [PubMed] [Google Scholar]
  3. Kiernan MC, Vucic S, Cheah BC, et al. Amyotrophic lateral sclerosis. Lancet 2011 ; 377 : 942–955. [CrossRef] [PubMed] [Google Scholar]
  4. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg lecture. Neurology 1980 ; 30 : 1303–1313. [Google Scholar]
  5. Mukherjee A, Chakravarty A. Spasticity mechanisms – for the clinician. Front Neurol 2010 ; 1 : 149. [CrossRef] [PubMed] [Google Scholar]
  6. Bennett DJ, Gorassini M, Fouad K, et al. Spasticity in rats with sacral spinal cord injury. J Neurotrauma 1999 ; 16 : 69–84. [CrossRef] [PubMed] [Google Scholar]
  7. Bellardita C, Caggiano V, Leiras R, et al. Spatiotemporal correlation of spinal network dynamics underlying spasms in chronic spinalized mice. Elife 2017 ; 13 : 6. [Google Scholar]
  8. Gillard PJ, Sucharew H, Kleindorfer et al. The negative impact of spasticity on the health-related quality of life of stroke survivors: a longitudinal cohort study. Health Qual Life Outcomes 2015 ; 13 : 159. [CrossRef] [PubMed] [Google Scholar]
  9. Elbasiouny SM, Moroz D, Bakr MM, Mushahwar VK. Management of spasticity after spinal cord injury: current techniques and future directions. Neurorehabil Neural Repair 2010 ; 24 : 23–33. [CrossRef] [PubMed] [Google Scholar]
  10. Eccles JC, Kostyuk PG, Schmidt RF. Presynaptic inhibition of the central actions of flexor reflex afferents. J Physiol 1962 ; 161 : 258–281. [CrossRef] [PubMed] [Google Scholar]
  11. Hultborn H, Jankowska E, Lindstrom S, Roberts W. Neuronal pathway of the recurrent facilitation of motoneurones. J Physiol 1971 ; 218 : 495–514. [CrossRef] [PubMed] [Google Scholar]
  12. Crone C, Nielsen J, Petersen N, et al. Disynaptic reciprocal inhibition of ankle extensors in spastic patients. Brain 1994 ; 117 : 1161–1168. [CrossRef] [PubMed] [Google Scholar]
  13. Lundberg A, Voorhoeve P. Effects from the pyramidal tract on spinal reflex arcs. Acta Physiol Scand 1962 ; 56 : 201–219. [CrossRef] [PubMed] [Google Scholar]
  14. Nielsen J, Petersen N, Ballegaard M, et al. H-reflexes are less depressed following muscle stretch in spastic spinal cord injured patients than in healthy subjects. Exp Brain Res 1993 ; 97 : 173–176. [CrossRef] [PubMed] [Google Scholar]
  15. Thompson FJ, Reier PJ, Lucas CC, Parmer R. Altered patterns of reflex excitability subsequent to contusion injury of the rat spinal cord. J Neurophysiol 1992 ; 68 : 1473–1486. [PubMed] [Google Scholar]
  16. Crone C, Johnsen LL, Biering-Sorensen F, Nielsen JB. Appearance of reciprocal facilitation of ankle extensors from ankle flexors in patients with stroke or spinal cord injury. Brain 2003 ; 126 : 495–507. [CrossRef] [PubMed] [Google Scholar]
  17. Jean-Xavier C, Mentis GZ, O’Donovan MJ, et al. Dual personality of GABA/glycine-mediated depolarizations in immature spinal cord. Proc Natl Acad Sci USA 2007 ; 104 : 11477–11482. [CrossRef] [Google Scholar]
  18. Boulenguez P, Liabeuf S, Bos R, et al. Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury. Nat Med 2010 ; 16 : 302–307. [CrossRef] [PubMed] [Google Scholar]
  19. Boulenguez P, Liabeuf S, Vinay L. Perte d’inhibition neuronale et spasticité après traumatisme de la moelle épinière. Med Sci (Paris) 2011 ; 27 : 7–9. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  20. Bos R, Sadlaoud K, Boulenguez P, et al. Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2. Proc Natl Acad Sci USA 2013 ; 110 : 348–353. [CrossRef] [Google Scholar]
  21. Jean-Xavier C, Pflieger JF, Liabeuf S, Vinay L. Inhibitory postsynaptic potentials in lumbar motoneurons remain depolarizing after neonatal spinal cord transection in the rat. J Neurophysiol 2006 ; 96 : 2274–2281. [CrossRef] [PubMed] [Google Scholar]
  22. Bouhadfane M, Tazerart S, Moqrich A, et al. Sodium-mediated plateau potentials in lumbar motoneurons of neonatal rats. J Neurosci 2013 ; 33 : 15626–15641. [CrossRef] [PubMed] [Google Scholar]
  23. Brocard F, Shevtsova NA, Bouhadfane M, et al. Activity-dependent changes in extracellular Ca2+ and K+ reveal pacemakers in the spinal locomotor-related network. Neuron 2013 ; 77 : 1047–1054. [CrossRef] [PubMed] [Google Scholar]
  24. Brocard F, Tazerart S, Vinay L. Do pacemakers drive the central pattern generator for locomotion in mammals ?. Neuroscientist 2010 ; 16 : 139–155. [CrossRef] [PubMed] [Google Scholar]
  25. Tazerart S, Vinay L, Brocard F. The persistent sodium current generates pacemaker activities in the central pattern generator for locomotion and regulates the locomotor rhythm. J Neurosci 2008 ; 28 : 8577–8589. [CrossRef] [PubMed] [Google Scholar]
  26. Tazerart S, Viemari JC, Darbon P, et al. Contribution of persistent sodium current to locomotor pattern generation in neonatal rats. J Neurophysiol 2007 ; 98 : 613–628. [CrossRef] [PubMed] [Google Scholar]
  27. Brocard C, Plantier V, Boulenguez P, et al. Cleavage of Na(+) channels by calpain increases persistent Na+ current and promotes spasticity after spinal cord injury. Nat Med 2016 ; 22 : 404–411. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  28. Gorassini MA, Knash ME, Harvey PJ, et al. Role of motoneurons in the generation of muscle spasms after spinal cord injury. Brain 2004 ; 127 : 2247–2258. [CrossRef] [PubMed] [Google Scholar]
  29. Guroff G. A neutral, calcium-activated proteinase from the soluble fraction of rat brain. J Biol Chem 1964 ; 239 : 149–155. [PubMed] [Google Scholar]
  30. Goll DE, Thompson VF, Li H, et al. The calpain system. Physiol Rev 2003 ; 83 : 731–801. [Google Scholar]
  31. Shumway SD, Maki M, Miyamoto S. The PEST domain of IkappaBalpha is necessary and sufficient for in vitro degradation by mu-calpain. J Biol Chem 1999 ; 274 : 30874–30881. [CrossRef] [PubMed] [Google Scholar]
  32. Baudry M, Bi X. Calpain-1 and calpain 2: The Yin and Yang of synaptic plasticity and neurodegeneration. Trends Neurosci 2016 ; 39 : 235–245. [CrossRef] [PubMed] [Google Scholar]
  33. Banik NL, Matzelle DC, Gantt-Wilford G, et al. Increased calpain content and progressive degradation of neurofilament protein in spinal cord injury. Brain Res 1997 ; 752 : 301–306. [CrossRef] [PubMed] [Google Scholar]
  34. Du S, Rubin A, Klepper S, et al. Calcium influx and activation of calpain I mediate acute reactive gliosis in injured spinal cord. Exp Neurol 1999 ; 157 : 96–105. [CrossRef] [PubMed] [Google Scholar]
  35. Arataki S, Tomizawa K, Moriwaki A, et al. Calpain inhibitors prevent neuronal cell death and ameliorate motor disturbances after compression-induced spinal cord injury in rats. J Neurotrauma 2005 ; 22 : 398–406. [CrossRef] [PubMed] [Google Scholar]
  36. Iwata A, Stys PK, Wolf JA, et al. Traumatic axonal injury induces proteolytic cleavage of the voltage-gated sodium channels modulated by tetrodotoxin and protease inhibitors. J Neurosci 2004 ; 24 : 4605–4613. [CrossRef] [PubMed] [Google Scholar]
  37. Armstrong CM, Bezanilla F, Rojas E. Destruction of sodium conductance inactivation in squid axons perfused with pronase. J Gen Physiol 1973 ; 62 : 375–391. [CrossRef] [PubMed] [Google Scholar]
  38. Puskarjov M, Ahmad F, Kaila K, Blaesse P. Activity-dependent cleavage of the K-Cl cotransporter KCC2 mediated by calcium-activated protease calpain. J Neurosci 2012 ; 32 : 11356–11364. [CrossRef] [PubMed] [Google Scholar]
  39. Zhou HY, Chen SR, Byun HS, et al. N-methyl-D-aspartate receptor- and calpain-mediated proteolytic cleavage of K+-Cl- cotransporter-2 impairs spinal chloride homeostasis in neuropathic pain. J Biol Chem 2012 ; 287 : 33853–33864. [CrossRef] [PubMed] [Google Scholar]
  40. Mercado A, Broumand V, Zandi-Nejad K, et al. A C-terminal domain in KCC2 confers constitutive K+-Cl- cotransport. J Biol Chem 2006 ; 281 : 1016–1026. [CrossRef] [PubMed] [Google Scholar]

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