Stephanie C. Gantz

This study characterizes the electrophysiological properties of hypothalamic A11 dopamine neurons in mice and shows that mu-opioid receptor activation reduces their pacemaking activity.

This study shows that GluD1R current is inhibited by extracellular protons in mouse serotonin neurons and that GluD1R-deficient mice show impaired CO2-induced behavioral responses.

The paper investigates how alpha2-adrenergic receptors modulate noradrenaline-dependent synaptic transmission in the dorsal raphe nucleus, showing that 2-AR inhibit noradrenaline release and reduce serotonin neuron activity.

The paper shows that tonic GluD1R channel current in the dorsal raphe nucleus is not influenced by G protein activity, suggesting a separate mechanism for its generation.

The paper shows that inhibitory chemogenetics using PSAM4-GlyR may activate D1-MSNs instead of inhibiting them, highlighting issues with using chloride conductances for neuronal inhibition.

The paper demonstrates that GluD1R functions as a constitutively active ion channel in dorsal raphe neurons, mediating 1-AR-induced inward current and pacemaker firing.