Abstract

Abstract ID 28219

Poster Board 545

Ion channel function of native delta glutamate receptors (GluD_Rs) is incompletely understood. Previously, we and others have shown that activation of G_q protein-coupled receptors (GPCR) produces a slow inward current carried by GluD1_R. GluD1_R 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 GluD1_R current. Neither augmentation nor disruption of G protein activity affected tonic GluD1_R current, suggesting that on-going G protein-coupled receptor activity does not give rise to tonic GluD1_R current. Further, tonic GluD1_R current was unaffected by the addition of external glycine or D-serine, which influence GluD2_R current at millimolar concentrations. Instead, GPCR-stimulated and tonic GluD1_R current is regulated by external calcium. In current-clamp recording, block of GluD1_R channels hyperpolarized the membrane by ∼10 mV at subthreshold potentials, reducing excitability. Thus, GluD1_R carry a G protein-independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus.