MECP2 regulates transcription of genes involved in GABA signaling

Mecp2 deletion in mouse GABAergic parvalbumin-expressing (PV) cells, cortical interneurons playing a key role in visual experience-induced ocular dominance plasticity, does not result in Rett-like phenotype, other than defects in motor coordination and motor learning. While functions of the visual cortex are preserved in mice lacking Mecp2 in GABAergic PV cells, the visual input-induced spiking responses are decreased. Mecp2 loss impairs maturation of membrane functions of cortical GABAergic PV cells. Mecp2 may be needed for PV cell-mediated cortical GABA inhibition. Mecp2-deficient cortical PV cells show reduced mRNA levels of several genes involved in GABA signaling, such as Parvalbumin, Gad2, Calretinin, Gabra1 and Gabra2, as well as reduced levels of Glu3, a glutamate receptor subunit, and Kv3.1, a potassium channel.