Loss of <i>Frrs1l</i> disrupts synaptic AMPA receptor function, and results in neurodevelopmental, motor, cognitive and electrographical abnormalities.

In Frrs1l −/− mice, we found a highly significant reduction in the levels of core AMPA receptor proteins from birth through to adulthood, and, importantly, AMPA receptor subunits lack complex glycosylation, indicating incomplete receptor maturation.

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