Regulation of seizure-induced MeCP2 Ser421 phosphorylation in the developing brain.

ABSTRACT: Neonatal seizures disrupt normal synaptic maturation and often lead to later-life epilepsy and cognitive deficits. During early life, the brain exhibits heightened synaptic plasticity, in part due to a developmental overabundance of Ca_V1.2 L-type voltage gated calcium (Ca²⁺) channels (LT-VGCCs) and Ca²⁺-permeable AMPARs (CP-AMPARs) lacking GluA2 subunits. We hypothesized that early-life seizures overactivate these channels, in turn dysregulating Ca²⁺-dependent signaling pathways including that of methyl CPG binding protein 2 (MeCP2), a transcription factor implicated in the autism spectrum disorder (ASD) Rett Syndrome. Here, we show that in vivo hypoxia-induced seizures (HS) in postnatal day (P)10 rats acutely induced phosphorylation of the neuro

SUBMITTER: Rosenberg EC 

PROVIDER: S-EPMC6745700 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature