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Parkinson's Disease and Related Disorders

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Atp1a3-deficient heterozygous mice under the stress showed shorter stride length relevant to symptoms of Rapid-onset dystonia parkinsonism

  • P2-308
  • 杉本 大樹 / Hiroki Sugimoto:1 川上 潔 / kiyoshi Kawakami:1 
  • 1:自治医大・分子病態・細胞生物 / Div Biol, Cent Mol Med, Jichi Med Univ, Tochigi, Japan 

Dystonia is a neurological disorder characterized by involuntary and simultaneous contractions of agonist and antagonist muscles. Rapid-onset dystonia parkinsonism (RDP) is one of the heredity forms of dystonia caused by mutations of Na,K-ATPase α3 subunit gene (ATP1A3). The abrupt onset of bulbar and limb symptoms of RDP is triggered by physical and/or emotional stress. Previously, we reported that Atp1a3-deficient heterozygous mice (Atp1a3+/-) showed prolonged dystonic postures compared with wild type by kainate injection into cerebellum, but never showed spontaneous movement disorder like RDP patients. In this study, we tested whether Atp1a3+/- elicit dystonia symptoms under chronic restraint stress.Atp1a3+/- exhibited shorter stride length at 4-week old without stress, and shorter stride length of Atp1a3+/- sustained under chronic restraint stress condition. Shorter hanging time of Atp1a3+/- the hanging box test which evaluates balance and grip strength was also observed after the stress loading. Reduced stride length and hanging time may be relevant to symptoms of RDP patients such as gait abnormality. Our results suggest that Atp1a3+/- will be a useful model animal to address a pathophysiology of movement abnormality of RDP.

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