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

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 Ca1.2 L-type voltage gated calcium (Ca) channels (LT-VGCCs) and Ca-permeable AMPARs (CP-AMPARs) lacking GluA2 subunits.

Development of later life spontaneous seizures in a rodent model of hypoxia-induced neonatal seizures.

Purpose: To study the development of epilepsy following hypoxia-induced neonatal seizures in Long-Evans rats and to establish the presence of spontaneous seizures in this model of early life seizures.

Methods: Long-Evans rat pups were subjected to hypoxia-induced neonatal seizures at postnatal day 10 (P10). Epidural cortical electroencephalography (EEG) and hippocampal depth electrodes were used to detect the presence of seizures in later adulthood (> P60).