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• W965367960 abstract "Mutations in the methyl-CpG-binding protein (MeCP2) have been linked as the causative factor to Rett Syndrome (RTT). The MECP2 gene encodes a DNA binding protein that binds to methylated cytosines in the mammalian genome. The disease-causing mutations found in RTT patients are predicted to result in the loss of function of MeCP2 that then results in genes turned on in an inappropriate manner. Over the past several years, our group has examined the role of MeCP2 in complex behavior as well as neurotransmission. Our behavioral analysis has shown that the forebrain-specific Mecp2 loss-of-function in mice could recapitulate several behavioral and neurological deficits associated with RTT. Interestingly, we could also show that brain region-specific Mecp2 loss-of-function, such as selective knock down of MeCP2 in basolateral amygdala, could trigger a subset of RTT phenotypes such as an increased anxiety-like behavior and deficits in cue-dependent fear conditioning. We have also demonstrated that loss of MeCP2 in neurons results in a decrease in spontaneous excitatory synaptic transmission coupled with an increase in action potential-driven excitatory drive. The combined effort of behavioral and synaptic analysis of MeCP2-associated phenotypes will not only open new avenues for understanding neuronal circuit abnormalities associated with neurodevelopmental disorders but also elucidate potential targets for addressing the pathophysiology of several intractable neuropsychiatric disorders." @default.
• W965367960 created "2016-06-24" @default.
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• W965367960 date "2012-01-01" @default.
• W965367960 modified "2023-09-25" @default.
• W965367960 title "Analysis of MeCP2 Function in the CNS" @default.
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• W965367960 doi "https://doi.org/10.1007/978-3-642-27913-3_11" @default.
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