The Gpr45-CreERT2 knock-in model was used to express chronic and acute actuators to the PVH to assess the role of PVH Gpr45 neurons in energy homeostasis.
First-pass extracted concept
PVH Gpr45 neurons
Aliases
Gpr45-expressing neurons in the PVH, PVH^Gpr45 neurons
Evidence Snippets
Supporting Sources
Linked Claims
Acute chemogenetic stimulation of PVH Gpr45 neurons durably suppresses food intake regardless of caloric need state or food palatability.
Targeted deletion of Gpr45 from the PVH phenocopies obesity and hyperphagia, supporting the PVH glutamatergic population as a major site of Gpr45 action.
Permanent silencing of PVH Gpr45 neurons with TeNT causes rapid weight gain and increased food intake, supporting a critical role for PVH Gpr45 neuronal activity in body-weight and appetite regulation.
Constitutive activation of PVH Gpr45 neurons with NaChBac has limited to no effect on body weight and food consumption, implying redundant circuitry may limit weight-loss effects.