Enhanced long-term potentiation in mature rats in a model of epileptic spasms with betamethasone-priming and postnatal N-methyl-D-aspartate administration.

This study is the first to provide a basis for the alteration of synaptic plasticity and transmission in a model of epileptic spasms of unknown cause. Postnatal NMDA treatment causing epileptic spasms-like aberrant episodes in the early stage of life in rats has a latent influence on various forms of synaptic plasticity in the hippocampus. Our results provide a novel insight into cognitive impairment that appears later in life in patients with a history of epileptic spasms.