Potentiation of neuronal activity by tonic GluD1 current in brain slices.

Daniel S Copeland, Aleigha Gugel, Stephanie C Gantz

EMBO reports 2023 Jul 05

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Ion channel function of native delta glutamate receptors (GluDR ) is incompletely understood. Previously, we and others have shown that activation of Gαq protein-coupled receptors (GqPCR) produces a slow inward current carried by GluD1R . GluD1R also carries a tonic cation current of unknown cause. Here, using voltage-clamp electrophysiological recordings from adult mouse brain slices containing the dorsal raphe nucleus, we find no role of ongoing G-protein-coupled receptor activity in generating or sustaining tonic GluD1R currents. Neither augmentation nor disruption of G protein activity affects tonic GluD1R currents, suggesting that ongoing G-protein-coupled receptor activity does not give rise to tonic GluD1R currents. Further, the tonic GluD1R current is unaffected by the addition of external glycine or D-serine, which influences GluD2R current at millimolar concentrations. Instead, GqPCR-stimulated and tonic GluD1R currents are regulated by physiological levels of external calcium. In current-clamp recordings, block of GluD1R channels hyperpolarizes the membrane by ~7 mV at subthreshold potentials, reducing excitability. Thus, GluD1R carries a G-protein-independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus. © 2023 The Authors. Published under the terms of the CC BY 4.0 license.

Citation

Daniel S Copeland, Aleigha Gugel, Stephanie C Gantz. Potentiation of neuronal activity by tonic GluD1 current in brain slices. EMBO reports. 2023 Jul 05;24(7):e56801