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GluK2 Q/R editing regulates kainate receptor signaling and long-term potentiation of AMPA receptors
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 ∼95% unedited GluK2(Q) to wild-type counterparts that express ∼85% ed...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10504484/ https://www.ncbi.nlm.nih.gov/pubmed/37720087 http://dx.doi.org/10.1016/j.isci.2023.107708 |
Sumario: | 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 ∼95% unedited GluK2(Q) to wild-type counterparts that express ∼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. |
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