Absence seizures and sleep-wake abnormalities in a rat model of GRIN2B neurodevelopmental disorder.

ABSTRACT:

Objective

Pathogenic mutations in GRIN2B are an important cause of severe neurodevelopmental disorders resulting in epilepsy, autism, and intellectual disability. GRIN2B encodes the GluN2B subunit of N-methyl-d-aspartate receptors (NMDARs), which are ionotropic glutamate receptors critical for normal development of the nervous system and synaptic plasticity. Here, we characterized a novel Grin2b heterozygous knockout rat model with electroencephalography (EEG) and pharmacological interventions to block spontaneous seizures.

Methods

Through western blot analysis we assessed the extent of GluN2B protein knockdown in knockout (Grin2b^+/-) rats compared to controls. We recorded 24-h wireless multi-channel EEG to test whether seizure activity was present and analyzed sl

SUBMITTER: Hristova K 

PROVIDER: S-EPMC12779324 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature