Rett　syndrome　is　a　neurodevelopmental　disorder　that　usually　arises　from　mutations　or　deletions　in　methyl-CpG　binding　protein　2　(MeCP2),　a　transcriptional　regulator　that　affects　neuronal　development　and　maturation　without　causing　cell　loss.　Here,　we　show　that　silencing　of　MeCP2　decreased　neurite　arborization　and　synaptogenesis　in　cultured　hippocampal　neurons　from　rat　fetal　brains.　These　structural　defects　were　associated　with　alterations　in　synaptic　transmission　and　neural　network　activity.　Similar　retardation　of　dendritic　growth　was　also　observed　in　MeCP2-deficient　newborn　granule　cells　in　the　dentate　gyrus　of　adult　mouse　brains　in　vivo,　demonstrating　direct　and　cell-autonomous　effects　on　individual　neurons.　These　defects,　caused　by　MeCP2　deficiency,　were　reversed　by　treatment　with　the　US　Food　and　Drug　Administration-approved　drug,　pentobarbital,　in　vitro　and　in　vivo,　possibly　caused　by　modulation　of　gamma-aminobutyric　acid　signaling.　The　results　indicate　that　drugs　modulating　gamma-aminobutyric　acid　signaling　are　potential　therapeutics　for　Rett　syndrome.