| First Author | Fourgeaud L | Year | 2010 |
| Journal | Proc Natl Acad Sci U S A | Volume | 107 |
| Issue | 51 | Pages | 22278-83 |
| PubMed ID | 21135233 | Mgi Jnum | J:167301 |
| Mgi Id | MGI:4867777 | Doi | 10.1073/pnas.0914064107 |
| Citation | Fourgeaud L, et al. (2010) MHC class I modulates NMDA receptor function and AMPA receptor trafficking. Proc Natl Acad Sci U S A 107(51):22278-83 |
| abstractText | Proteins of the major histocompatibility complex class I (MHCI) are known for their role in immunity and have recently been implicated in long-term plasticity of excitatory synaptic transmission. However, the mechanisms by which MHCI influences synaptic plasticity remain unknown. Here we show that endogenous MHCI regulates synaptic responses mediated by NMDA-type glutamate receptors (NMDARs) in the mammalian central nervous system (CNS). The AMPA/NMDA ratio is decreased at MHCI-deficient hippocampal synapses, reflecting an increase in NMDAR-mediated currents. This enhanced NMDAR response is not associated with changes in the levels, subunit composition, or gross subcellular distribution of NMDARs. Increased NMDAR-mediated currents in MHCI-deficient neurons are associated with characteristic changes in AMPA receptor trafficking in response to NMDAR activation. Thus, endogenous MHCI tonically inhibits NMDAR function and controls downstream NMDAR-induced AMPA receptor trafficking during the expression of plasticity. |
