| First Author | Nair JD | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 10 | Pages | 107708 |
| PubMed ID | 37720087 | Mgi Jnum | J:340818 |
| Mgi Id | MGI:7530455 | Doi | 10.1016/j.isci.2023.107708 |
| Citation | Nair JD, et al. (2023) GluK2 Q/R editing regulates kainate receptor signaling and long-term potentiation of AMPA receptors. iScience 26(10):107708 |
| abstractText | Q/R editing of the kainate receptor (KAR) subunit GluK2 radically alters recombinant KAR properties, but the effects on endogenous KARs in vivo remain largely unexplored. Here, we compared GluK2 editing-deficient mice that express approximately 95% unedited GluK2(Q) to wild-type counterparts that express approximately 85% edited GluK2(R). At mossy fiber-CA3 (MF-CA3) synapses GluK2(Q) mice displayed increased postsynaptic KAR function and KAR-mediated presynaptic facilitation, demonstrating enhanced ionotropic function. Conversely, GluK2(Q) mice exhibited reduced metabotropic KAR function, assessed by KAR-mediated inhibition of slow after-hyperpolarization currents (I(SAHP)). GluK2(Q) mice also had fewer GluA1-and GluA3-containing AMPA receptors (AMPARs) and reduced postsynaptic AMPAR currents at both MF-CA3 and CA1-Schaffer collateral synapses. Moreover, long-term potentiation of AMPAR-mediated transmission at CA1-Schaffer collateral synapses was reduced in GluK2(Q) mice. These findings suggest that GluK2 Q/R editing influences ionotropic/metabotropic balance of KAR signaling to regulate synaptic expression of AMPARs and plasticity. |
