Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice

Abstract The neural basis of anxiety is unclear, which hinders the treatment of anxiety disorders. Here, we found that αCaMKII+ neurons in the medial prefrontal cortex (mPFCαCaMKII+) responded to stressors with increased activity both under physiological conditions and after repeated restraint stres...

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Main Authors: Liu Yang, Meng Zhang, Xiaomin Sun, Anqi Du, Jiajia Jia, Nan Li, Gonghui Hu, Yingchang Lu, Sihan Wang, Jingsai Zhang, Wenjie Chen, Hanbing Yu, Yu Zhou
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-07802-9
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author Liu Yang
Meng Zhang
Xiaomin Sun
Anqi Du
Jiajia Jia
Nan Li
Gonghui Hu
Yingchang Lu
Sihan Wang
Jingsai Zhang
Wenjie Chen
Hanbing Yu
Yu Zhou
author_facet Liu Yang
Meng Zhang
Xiaomin Sun
Anqi Du
Jiajia Jia
Nan Li
Gonghui Hu
Yingchang Lu
Sihan Wang
Jingsai Zhang
Wenjie Chen
Hanbing Yu
Yu Zhou
author_sort Liu Yang
collection DOAJ
description Abstract The neural basis of anxiety is unclear, which hinders the treatment of anxiety disorders. Here, we found that αCaMKII+ neurons in the medial prefrontal cortex (mPFCαCaMKII+) responded to stressors with increased activity both under physiological conditions and after repeated restraint stress (RRS) in mice. Chemogenetic activation of mPFCαCaMKII+ neurons ameliorated stress-induced anxiety. A delayed increase in the expression of growth hormone secretagogue receptor 1a (GHS-R1a), the receptor of the peripheral metabolic hormone ghrelin, in mPFCαCaMKII+ neurons coincided with reduced excitatory synaptic transmission and the development of RRS-induced enhancement of anxiety-related behavior. Virus-mediated GHS-R1a upregulation in mPFCαCaMKII+ neurons exaggerated the excitation/inhibition (E/I) imbalance and promoted anxiety-related behavior, whereas GHS-R1a knockdown had the opposite effect. We conclude that GHS-R1a signaling contributes to the development of stress-induced anxiety by shaping synaptic activity of mPFCαCaMKII+ neurons. GHS-R1a may be a new therapeutic target for treating anxiety disorders.
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spelling doaj-art-88e247e7d6c245709367fa5148b42fc02025-08-20T03:53:32ZengNature PortfolioCommunications Biology2399-36422025-03-018111210.1038/s42003-025-07802-9Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in miceLiu Yang0Meng Zhang1Xiaomin Sun2Anqi Du3Jiajia Jia4Nan Li5Gonghui Hu6Yingchang Lu7Sihan Wang8Jingsai Zhang9Wenjie Chen10Hanbing Yu11Yu Zhou12Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Health and Life Sciences, University of Health and Rehabilitation SciencesDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Qingdao UniversityAbstract The neural basis of anxiety is unclear, which hinders the treatment of anxiety disorders. Here, we found that αCaMKII+ neurons in the medial prefrontal cortex (mPFCαCaMKII+) responded to stressors with increased activity both under physiological conditions and after repeated restraint stress (RRS) in mice. Chemogenetic activation of mPFCαCaMKII+ neurons ameliorated stress-induced anxiety. A delayed increase in the expression of growth hormone secretagogue receptor 1a (GHS-R1a), the receptor of the peripheral metabolic hormone ghrelin, in mPFCαCaMKII+ neurons coincided with reduced excitatory synaptic transmission and the development of RRS-induced enhancement of anxiety-related behavior. Virus-mediated GHS-R1a upregulation in mPFCαCaMKII+ neurons exaggerated the excitation/inhibition (E/I) imbalance and promoted anxiety-related behavior, whereas GHS-R1a knockdown had the opposite effect. We conclude that GHS-R1a signaling contributes to the development of stress-induced anxiety by shaping synaptic activity of mPFCαCaMKII+ neurons. GHS-R1a may be a new therapeutic target for treating anxiety disorders.https://doi.org/10.1038/s42003-025-07802-9
spellingShingle Liu Yang
Meng Zhang
Xiaomin Sun
Anqi Du
Jiajia Jia
Nan Li
Gonghui Hu
Yingchang Lu
Sihan Wang
Jingsai Zhang
Wenjie Chen
Hanbing Yu
Yu Zhou
Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
Communications Biology
title Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
title_full Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
title_fullStr Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
title_full_unstemmed Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
title_short Stress-induced GHS-R1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
title_sort stress induced ghs r1a expression in medial prefrontal cortical neurons promotes vulnerability to anxiety in mice
url https://doi.org/10.1038/s42003-025-07802-9
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