Calpain fosters the hyperexcitability of motoneurons after spinal cord injury and leads to spasticity.

ABSTRACT: Up-regulation of the persistent sodium current (I_NaP) and down-regulation of the potassium/chloride extruder KCC2 lead to spasticity after spinal cord injury (SCI). We here identified calpain as the driver of the up- and down-regulation of I_NaP and KCC2, respectively, in neonatal rat lumbar motoneurons. Few days after SCI, neonatal rats developed behavioral signs of spasticity with the emergence of both hyperreflexia and abnormal involuntary muscle contractions on hindlimbs. At the same time, in vitro isolated lumbar spinal cords became hyperreflexive and displayed numerous spontaneous motor outputs. Calpain-I expression paralleled with a proteolysis of voltage-gated sodium (Nav) channels and KCC2. Acute inhibition of calpains reduced this proteolysis, r

SUBMITTER: Plantier V 

PROVIDER: S-EPMC6927741 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature