Improvement of cerebellar ataxic gait by injecting Cbln1 into the cerebellum of cbln1-null mice.

ABSTRACT: Patients and rodents with cerebellar damage display ataxic gaits characterized by impaired coordination of limb movements. Here, gait ataxia in mice with a null mutation of the gene for the cerebellin 1 precursor protein (cbln1-null mice) was investigated by kinematic analysis of hindlimb movements during locomotion. The Cbln1 protein is predominately produced and secreted from cerebellar granule cells. The cerebellum of cbln1-null mice is characterized by an 80% reduction in the number of parallel fiber-Purkinje cell synapses compared with wild-type mice. Our analyses identified prominent differences in the temporal parameters of locomotion between cbln1-null and wild-type mice. The cbln1-null mice displayed abnormal hindlimb movements that were characterized by excessive toe elevation du

SUBMITTER: Takeuchi E 

PROVIDER: S-EPMC5906462 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature