Potentiation of neuronal activity by tonic GluD1 current in brain slices
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ABSTRACT: Ion channel function of native delta glutamate receptors (GluDRs) 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 carry 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 on-going 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 on-going 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 influence 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 carry a G protein-independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus.
SUBMITTER: Mr. Daniel, S Copeland
PROVIDER: S-SCDT-10_15252-EMBR_202356801 | biostudies-other |
REPOSITORIES: biostudies-other
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