Exon 5 and Spermine Regulate Deactivation of NMDA Receptor Subtypes

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Abstract
Deactivation of N-methyl-d-aspartate (NMDA) channels after brief agonist exposure determines the duration of their synaptic activation during excitatory neurotransmission. We performed patch-clamp recordings of l-glutamate responses from human embryonic kidney tumoral cells (HEK293) expressing NR1 subunit variants lacking exon 5 together with the NR2B subunit. These responses had deactivation components that lasted several seconds. The presence of exon 5 or spermine greatly accelerated deactivation ofl-glutamate responses through alterations in desensitization. These effects were also observed at positive holding potentials and in the presence of physiological Mg2+. Thus NR1 splicing and polyamines may have profound effects on the kinetics of NMDA receptor–mediated synaptic transmission.