| First Author | Ebralidze AK | Year | 1996 |
| Journal | J Neurosci | Volume | 16 |
| Issue | 16 | Pages | 5014-25 |
| PubMed ID | 8756432 | Mgi Jnum | J:34597 |
| Mgi Id | MGI:82052 | Doi | 10.1523/JNEUROSCI.16-16-05014.1996 |
| Citation | Ebralidze AK, et al. (1996) Modification of NMDA receptor channels and synaptic transmission by targeted disruption of the NR2C gene. J Neurosci 16(16):5014-25 |
| abstractText | A novel strain of mutant mouse has been generated with a deletion of the gene encoding the NR2C subunit of the NMDA receptor, which is primarily expressed in cerebellar granule cells. Patch-clamp recordings from granule cells in thin cerebellar slices were used to assess the consequences of the gene deletion. In granule cells of wild-type animals, a wide range of single-channel conductances were observed (19-60 pS). The disruption of the NR2C gene results in the disappearance of low-conductance NMDA receptor channels ( < 37 pS) normally expressed in granule cells during developmental maturation. The NMDA receptor-mediated synaptic current is markedly potentiated in amplitude, but abbreviated in duration (with no net difference in total charge), and the non-NMDA component of the synaptic current was reduced. We conclude that the NR2C subunit contributes to functional heteromeric NMDA receptor-subunit assemblies at the mossy fiber synapse and extrasynaptic sites during maturation, and the conductance level exhibited by a given receptor macromolecule may reflect the stochiometry of subunit composition. |
