Abstract
AbstractMechanisms of specific memory deficits associated with Rett syndrome are poorly understood, at least in part because mutations ofMECP2have confounding effects on nervous system development and basal synaptic transmission. To mitigate such empirical uncertainties, this study exploited technical advantages of theAplysiasensorimotor synapse to examine the potential role of MeCP2 in long-term synaptic plasticity. The results indicate MeCP2 may act as an inhibitory constraint on gene expression required for formation as well as maintenance of plasticity.
Publisher
Cold Spring Harbor Laboratory