Calretinin and Neuropeptide Y interneurons are differentially altered in the motor cortex of the SOD1^G93A mouse model of ALS.

ABSTRACT: Increasing evidence indicates an excitatory/inhibitory imbalance may have a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). Impaired inhibitory circuitry is consistently reported in the motor cortex of both familial and sporadic patients, closely associated with cortical hyperexcitability and ALS onset. Inhibitory network dysfunction is presumably mediated by intra-cortical inhibitory interneurons, however, the exact cell types responsible are yet to be identified. In this study we demonstrate dynamic changes in the number of calretinin- (CR) and neuropeptide Y-expressing (NPY) interneurons in the motor cortex of the familial hSOD1^G93A ALS mouse model, suggesting their potential involvement in motor neuron circuitry defects. We show that the density of

SUBMITTER: Clark RM 

PROVIDER: S-EPMC5353592 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature