GHS-R1a signaling drives anxiety-related behavior by shaping excitability of ventromedial hypothalamic neurons.

ABSTRACT: The neural substrates of anxiety are poorly understood, which hinders treatment of anxiety disorders. Here we found, αCaMKII⁺ neurons in the ventral medial hypothalamic nucleus (VMH) responded to stressors with increased activity in male mice, both under physiological conditions and after repeated restraint stress. Activation of VMH αCaMKII⁺ neurons were necessary and sufficient to ameliorate stress-induced anxiety. The peripheral metabolic hormone ghrelin and receptor GHS-R1a play a complex role in emotion regulation; however, the mechanism is uncertain. A delayed increase in GHS-R1a expression in VMH αCaMKII⁺ neurons coincided with the development of stress-induced enhancement of anxiety-related behavior. GHS-R1a expression in VMH αCaMKII⁺ neur

SUBMITTER: Zhang M 

PROVIDER: S-EPMC12022087 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature