Regulation of Neuronal Activity by GluD1 Current in Brain Slices

Abstract ID 28219 Poster Board 545 Ion channel function of native delta glutamate receptors (GluDRs) is incompletely understood. Previously, we and others have shown that activation of Gq protein-coupled receptors (GPCR) produces a slow inward current carried by GluD1R. GluD1R also carry a tonic cat...

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Veröffentlicht in:The Journal of pharmacology and experimental therapeutics 2023-06, Vol.385, p.545-545
Hauptverfasser: Gantz, Stephanie, Copeland, Daniel, Gugel, Aleigha
Format: Artikel
Sprache:eng
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Zusammenfassung:Abstract ID 28219 Poster Board 545 Ion channel function of native delta glutamate receptors (GluDRs) is incompletely understood. Previously, we and others have shown that activation of Gq protein-coupled receptors (GPCR) produces a slow inward current carried by GluD1R. GluD1R also carry a tonic cation current of unknown origin. Here, using voltage-clamp electrophysiological recordings from adult male and female mouse brain slices containing the dorsal raphe nucleus, we find no role of on-going G protein-coupled receptor activity in generating or sustaining tonic GluD1R current. Neither augmentation nor disruption of G protein activity affected tonic GluD1R current, suggesting that on-going G protein-coupled receptor activity does not give rise to tonic GluD1R current. Further, tonic GluD1R current was unaffected by the addition of external glycine or D-serine, which influence GluD2R current at millimolar concentrations. Instead, GPCR-stimulated and tonic GluD1R current is regulated by external calcium. In current-clamp recording, block of GluD1R channels hyperpolarized the membrane by ∼10 mV at subthreshold potentials, reducing excitability. Thus, GluD1R carry a G protein-independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus.
ISSN:0022-3565
DOI:10.1124/jpet.122.282190