Experience-dependent retinogeniculate synapse remodeling is abnormal in MeCP2-deficient mice.

ABSTRACT: Mutations in MECP2 underlie the neurodevelopmental disorder Rett syndrome (RTT). One hallmark of RTT is relatively normal development followed by a later onset of symptoms. Growing evidence suggests an etiology of disrupted synaptic function, yet it is unclear how these abnormalities explain the clinical presentation of RTT. Here we investigate synapse maturation in Mecp2-deficient mice at a circuit with distinct developmental phases: the retinogeniculate synapse. We find that synapse development in mutants is comparable to that of wild-type littermates between postnatal days 9 and 21, indicating that initial phases of synapse formation, elimination, and strengthening are not significantly affected by MeCP2 absence. However, during the subsequent experience-dependent phase of synapse remod

SUBMITTER: Noutel J 

PROVIDER: S-EPMC3082316 | biostudies-literature | 2011 Apr

REPOSITORIES: biostudies-literature