Exon 5 and spermine regulate deactivation of NMDA receptor subtypes.
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 of L-glutamate responses through alterations in desensitization. These effects were also observed at positive holding potentials and in the presence of physiological Mg(2+). Thus NR1 splicing and polyamines may have profound effects on the kinetics of NMDA receptor-mediated synaptic transmission.
Rumbaugh
G
G
Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007, USA.
Prybylowski
K
K
Wang
J F
JF
Vicini
S
S
D002460:Cell Line; D004594:Electrophysiology; D005091:Exons / Q000502:physiology*; D006801:Humans; D008274:Magnesium / Q000502:physiology; D018408:Patch-Clamp Techniques; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000502:physiology*; D011994:Recombinant Proteins; D013096:Spermine / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D014162:Transfection
D016194:Receptors, N-Methyl-D-Aspartate; D011994:Recombinant Proteins; D013096:Spermine; D008274:Magnesium