An aetiological Foxp2 mutation causes aberrant striatal activity and alters plasticity during skill learning.

ABSTRACT: Mutations in the human FOXP2 gene cause impaired speech development and linguistic deficits, which have been best characterised in a large pedigree called the KE family. The encoded protein is highly conserved in many vertebrates and is expressed in homologous brain regions required for sensorimotor integration and motor-skill learning, in particular corticostriatal circuits. Independent studies in multiple species suggest that the striatum is a key site of FOXP2 action. Here, we used in vivo recordings in awake-behaving mice to investigate the effects of the KE-family mutation on the function of striatal circuits during motor-skill learning. We uncovered abnormally high ongoing striatal activity in mice carrying an identical mutation to that of the KE family. Furthermore, there were drama

SUBMITTER: French CA 

PROVIDER: S-EPMC3481071 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature