{"title":"星状神经节阻滞通过抑制杏仁核基底外侧神经回路的蓝斑,减少小鼠条件性恐惧记忆的巩固。","authors":"Ziheng Wang, Zhouliang Liu, Youjia Yu, Yuning Sun, Yan Zhang, Kailun Gao, Junli Cao, Liwei Wang, Yangzi Zhu","doi":"10.1038/s41398-025-03383-7","DOIUrl":null,"url":null,"abstract":"<p><p>Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LC<sup>NE</sup>)-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LC<sup>NE</sup>-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"172"},"PeriodicalIF":6.2000,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085701/pdf/","citationCount":"0","resultStr":"{\"title\":\"Stellate ganglion block diminishes consolidation of conditioned fear memory in mice by inhibiting the locus coeruleus to the basolateral amygdala neural circuit.\",\"authors\":\"Ziheng Wang, Zhouliang Liu, Youjia Yu, Yuning Sun, Yan Zhang, Kailun Gao, Junli Cao, Liwei Wang, Yangzi Zhu\",\"doi\":\"10.1038/s41398-025-03383-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LC<sup>NE</sup>)-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LC<sup>NE</sup>-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.</p>\",\"PeriodicalId\":23278,\"journal\":{\"name\":\"Translational Psychiatry\",\"volume\":\"15 1\",\"pages\":\"172\"},\"PeriodicalIF\":6.2000,\"publicationDate\":\"2025-05-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085701/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Translational Psychiatry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41398-025-03383-7\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PSYCHIATRY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Psychiatry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41398-025-03383-7","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PSYCHIATRY","Score":null,"Total":0}
Stellate ganglion block diminishes consolidation of conditioned fear memory in mice by inhibiting the locus coeruleus to the basolateral amygdala neural circuit.
Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LCNE)-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LCNE-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.