MeCP2 represses the induction and maintenance of long-term synaptic plasticity

Abstract

Mechanisms of specific memory deficits associated with Rett syndrome are poorly understood, at least in part because mutations of MECP2 have confounding effects on nervous system development and basal synaptic transmission. To mitigate such empirical uncertainties, this study exploited technical advantages of the Aplysia sensorimotor 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.