Synaptic NMDA receptors in basolateral amygdala principal neurons are triheteromeric proteins: physiological role of GluN2B subunits

Delaney, Andrew J., Sedlak, Petra L., Autuori, Eleonora, Power, John M. and Sah, Pankaj (2013) Synaptic NMDA receptors in basolateral amygdala principal neurons are triheteromeric proteins: physiological role of GluN2B subunits. Journal of Neurophysiology, 109 5: 1391-1402. doi:10.1152/jn.00176.2012


Author Delaney, Andrew J.
Sedlak, Petra L.
Autuori, Eleonora
Power, John M.
Sah, Pankaj
Title Synaptic NMDA receptors in basolateral amygdala principal neurons are triheteromeric proteins: physiological role of GluN2B subunits
Journal name Journal of Neurophysiology   Check publisher's open access policy
ISSN 0022-3077
1522-1598
Publication date 2013-03-01
Year available 2012
Sub-type Article (original research)
DOI 10.1152/jn.00176.2012
Open Access Status DOI
Volume 109
Issue 5
Start page 1391
End page 1402
Total pages 12
Place of publication Bethesda, MD, United States
Publisher American Physiological Society
Collection year 2013
Language eng
Formatted abstract
N-methyl-ᴅ-aspartate (NMDA) receptors are heteromultimeric ion channels that contain an essential GluN1 subunit and two or more GluN2 (GluN2A–GluN2D) subunits. The biophysical properties and physiological roles of synaptic NMDA receptors are dependent on their subunit composition. In the basolateral amygdala (BLA), it has been suggested that the plasticity that underlies fear learning requires activation of heterodimeric receptors composed of GluN1/GluN2B subunits. In this study, we investigated the subunit composition of NMDA receptors present at synapses on principal neurons in the BLA. Purification of the synaptic fraction showed that both GluN2A and GluN2B subunits are present at synapses, and co-immunoprecipitation revealed the presence of receptors containing both GluN2A and GluN2B subunits. The kinetics of NMDA receptor-mediated synaptic currents and pharmacological blockade indicate that heterodimeric GluN1/GluN2B receptors are unlikely to be present at glutamatergic synapses on BLA principal neurons. Selective RNA interference-mediated knockdown of GluN2A subunits converted synaptic receptors to a GluN1/GluN2B phenotype, whereas knockdown of GluN2B subunits had no effect on the kinetics of the synaptically evoked NMDA current. Blockade of GluN1/GluN2B heterodimers with ifenprodil had no effect, but knockdown of GluN2B disrupted the induction of CaMKII-dependent long-term potentiation at these synapses. These results suggest that, on BLA principal neurons, GluN2B subunits are only present as GluN1/GluN2A/GluN2B heterotrimeric NMDA receptors. The GluN2B subunit has little impact on the kinetics of the receptor, but is essential for the recruitment of signaling molecules essential for synaptic plasticity.
Keyword LTP
Calcium
GluN2B
GluN2A
Memory
CaMKII
Long-term potentiation
D-aspartate receptor
Lateral amygdala
Conditioned fear
Nr2B subunit
Hippocampal synapses
Glutamate receptors
Visual-cortex
Rat
Expression
ᴅ-aspartate receptor
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published online before print: 5 December 2012.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2013 Collection
 
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Created: Wed, 13 Feb 2013, 01:42:53 EST by Debra McMurtrie on behalf of Queensland Brain Institute