Auteurs

Salmi M - Del Gallo F - Minlebaev M - Zakharov A - Pauly V - Perron P - Pons-Bennaceur A - Corby-Pellegrino S - Aniksztejn L - Lenck-Santini PP - Epsztein J - Khazipov R - Burnashev N - Bertini G - Szepetowski P

Journal

Epilepsia

Abstract

Glutamate-gated N-methyl-d-aspartate receptors (NMDARs) are instrumental to brain development and functioning. Defects in the GRIN2A gene, encoding the GluN2A subunit of NMDARs, cause slow-wave sleep (SWS)-related disorders of the epilepsy-aphasia spectrum (EAS). The as-yet poorly understood developmental sequence of early EAS-related phenotypes, and the role of GluN2A-containing NMDARs in the development of SWS and associated electroencephalographic (EEG) activity patterns, were investigated in Grin2a knockout (KO) mice.

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