[Calpain as a new therapeutic target for treating spasticity after a spinal cord injury]. / Une nouvelle cible thérapeutique dans le traitement de la spasticité après une lésion de la moelle épinière : la calpaïne.
Med Sci (Paris)
; 33(6-7): 629-636, 2017.
Article
em Fr
| MEDLINE
| ID: mdl-28990565
ABSTRACT
After a spinal cord injury (SCI), patients develop spasticity, a motor disorder characterized by hyperreflexia and stiffness of muscles. Spasticity results from alterations in motoneurons with an upregulation of their persistent sodium current (I NaP), simultaneously with a disinhibition caused by a reduction of expression of chloride (Cl-) co-transporters KCC2. Until recently the origin of alterations was unknown. After reviewing pathophysiology of spasticity, the manuscript relates our recent work showing a tight relationship between the calpain-dependent proteolysis of voltage-gated sodium channels, the upregulation of I NaP and spasticity following SCI. We also discuss KCC2 as a substrate of calpains which may contribute to the disinhibition of motoneurons below the lesion. This led us to consider the proteolytic cleavage of both sodium channels and KCC2 as the upstream mechanism contributing to the development of spasticity after SCI.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Traumatismos da Medula Espinal
/
Calpaína
/
Terapia de Alvo Molecular
/
Espasticidade Muscular
Tipo de estudo:
Etiology_studies
Limite:
Animals
/
Humans
Idioma:
Fr
Revista:
Med Sci (Paris)
Assunto da revista:
MEDICINA
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
França