AbstractIon 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. GluD1Ralso 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 GluD1Rcurrents. Neither augmentation nor disruption of G protein activity affects tonic GluD1Rcurrents, suggesting that ongoing G‐protein‐coupled receptor activity does not give rise to tonic GluD1Rcurrents. Further, the tonic GluD1Rcurrent is unaffected by the addition of external glycine or D‐serine, which influences GluD2Rcurrent at millimolar concentrations. Instead, GqPCR‐stimulated and tonic GluD1Rcurrents are regulated by physiological levels of external calcium. In current‐clamp recordings, block of GluD1Rchannels hyperpolarizes the membrane by ~7 mV at subthreshold potentials, reducing excitability. Thus, GluD1Rcarries a G‐protein‐independent tonic current that contributes to subthreshold neuronal excitation in the dorsal raphe nucleus.