{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang M"],"funding":["Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation)","Natural Science Foundation of Shandong Province","National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["3858"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12022087"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["The neural substrates of anxiety are poorly understood, which hinders treatment of anxiety disorders. Here we found, αCaMKII<sup>+</sup> 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<sup>+</sup> 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<sup>+</sup> neurons coincided with the development of stress-induced enhancement of anxiety-related behavior. GHS-R1a expression in VMH αCaMKII<sup>+</sup> neur"],"journal":["Nature communications"],"pubmed_title":["GHS-R1a signaling drives anxiety-related behavior by shaping excitability of ventromedial hypothalamic neurons."],"pmcid":["PMC12022087"],"funding_grant_id":["ZR2019ZD34","91732110","32071141","32371211"],"pubmed_authors":["Yang J","Yu M","Yang L","Zhang J","Lu Y","Wang C","Zhang M","Sun X","Zhou Y","Yu H","Li N","Mi X","Li X","Hu G","Wang S","Niu M","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"GHS-R1a signaling drives anxiety-related behavior by shaping excitability of ventromedial hypothalamic neurons.","description":"The neural substrates of anxiety are poorly understood, which hinders treatment of anxiety disorders. Here we found, αCaMKII<sup>+</sup> 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<sup>+</sup> 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<sup>+</sup> neurons coincided with the development of stress-induced enhancement of anxiety-related behavior. GHS-R1a expression in VMH αCaMKII<sup>+</sup> neur","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-01T03:05:48.554Z","creation":"2025-07-01T03:05:48.554Z"},"accession":"S-EPMC12022087","cross_references":{"pubmed":["40274845"],"doi":["10.1038/s41467-025-59116-3"]}}