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Potentiation of neuronal activity by tonic GluD1 current in brain slices
Journal article   Open access   Peer reviewed

Potentiation of neuronal activity by tonic GluD1 current in brain slices

Daniel S Copeland, Aleigha Gugel and Stephanie C Gantz
EMBO reports, Vol.24(7), e56801
05/08/2023
DOI: 10.15252/embr.202356801
PMCID: PMC10328076
PMID: 37154294
Appears in  UI Libraries Support Open Access
url
https://doi.org/10.15252/embr.202356801View
Published (Version of record) Open Access

Abstract

Ion channel function of native delta glutamate receptors (GluD ) is incompletely understood. Previously, we and others have shown that activation of Gαq protein-coupled receptors (GqPCR) produces a slow inward current carried by GluD1 . GluD1 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 GluD1 currents. Neither augmentation nor disruption of G protein activity affects tonic GluD1 currents, suggesting that ongoing G-protein-coupled receptor activity does not give rise to tonic GluD1 currents. Further, the tonic GluD1 current is unaffected by the addition of external glycine or D-serine, which influences GluD2 current at millimolar concentrations. Instead, GqPCR-stimulated and tonic GluD1 currents are regulated by physiological levels of external calcium. In current-clamp recordings, block of GluD1 channels hyperpolarizes the membrane by ~7 mV at subthreshold potentials, reducing excitability. Thus, GluD1 carries a G-protein-independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus.
 cation channel delta glutamate tonic current GluD G protein UIOWA OA Agreement

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