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Neurodevelopmental disorders are marked by inappropriate synaptic connectivity early in life, but how disruption of experience-dependent plasticity contributes to cognitive and behavioural decline in adulthood is unclear. Download Driver Wireless Asus Sonicmaster. Here we show that pup gathering behaviour and associated auditory cortical plasticity are impaired in female Mecp2 het mice, a model of Rett syndrome. In response to learned maternal experience, Mecp2 het females exhibited transient changes to cortical inhibitory networks typically associated with limited plasticity. Averting these changes in Mecp2 het through genetic or pharmacological manipulations targeting the GABAergic network restored gathering behaviour. We propose that pup gathering learning triggers a transient epoch of inhibitory plasticity in auditory cortex that is dysregulated in Mecp2 het. In this window of heightened sensitivity to sensory and social cues, Mecp2 mutations suppress adult plasticity independently from their effects on early development. Free Print To Pdf Creator.

Rett syndrome (RTT) is a neuropsychiatric disorder predominantly caused by mutations in the X-linked gene methyl CpG-binding protein 2 ( MECP2). Males with mutations of their single copy of the gene suffer neonatal encephalopathy and die in infancy, and most surviving patients with RTT are females that are heterozygous for Mecp2 mutations. In these females, random X-chromosome inactivation leads to mosaic wild type MECP2 expression and consequently a syndromic phenotype. Patients with RTT achieve early postnatal developmental milestones, but experience an abrupt developmental regression around 6–12 months. They typically survive into middle age, exhibiting sensory, cognitive and motor deficits throughout life. MECP2 is broadly expressed in the developing and adult brain, and is continually required to maintain adult neural function. Moreover, restoration of normal MECP2 expression in adult mice improves symptoms.