Assessing oligodendrocyte and myelin alterations following absence seizures in a rat model of GRIN2B neurodevelopmental disorder.

Neuronal activity can modulate myelination throughout life, influencing circuit function and behaviour. Pathological changes in neuronal activity have been associated with myelin remodelling in a rat model of idiopathic absence seizures, raising the question of whether this represents a common mechanism underlying absence epilepsy. Here we examined oligodendrocyte populations and myelin architecture in a rat model of GRIN2B neurodevelopmental disorder, a rare and severe condition that is frequently accompanied by absence seizures. Using histology and 3D imaging, we report that despite robust seizure-like activity in this model, there was no evidence of changes in oligodendrocyte lineage cell populations, overall myelin content, or node of Ranvier organization. These results contrast with prior reports of seizure-associated myelin modulation, indicating that seizure-induced myelin plasticity may not be a uniform feature across all models of absence seizures. Our findings indicate that such adaptations may depend on additional factors including seizure burden and timing, highlighting the need for further analysis to determine when and how myelin plasticity contributes to absence epilepsy.