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The dorsal raphe nucleus is the predominant source of central serotonin, where neuronal activity regulates complex emotional behaviors. Action potential firing of serotonin dorsal raphe neurons is driven via α1-adrenergic receptors (α1-A R ) activation. Despite this crucial role, the ion channels responsible for α1-A R -mediated depolarization are unknown. Here, we show in mouse brain slices that α1-A R -mediated excitatory synaptic transmission is mediated by the ionotropic glutamate receptor homolog cation channel, delta glutamate receptor 1 (GluD1). GluD1 R -channels are constitutively active under basal conditions carrying tonic inward current and synaptic activation of α1-A R s augments tonic GluD1 R -channel current. Further, loss of dorsal raphe GluD1 R -channels produces an anxiogenic phenotype. Thus, GluD1 R -channels are responsible for α1-A R -dependent induction of persistent pacemaker-type firing of dorsal raphe neurons and regulate dorsal raphe-related behavior. Given the widespread distribution of these channels, ion channel function of GluD1 R  as a regulator of neuronal excitability is proposed to be widespread in the nervous system.

Delta glutamate receptor conductance drives excitation of mouse dorsal raphe neurons