Fei Li , Zi-Ang Li , Jia Li , Hui-Min Tian , Dong-Ning Li , Zhong-Yi Liu , Jin Cheng , Tian-Yu Zhao , Li-Ming Liu , Yao-Hua Liu , Sha-Sha Tao , Fen-Sheng Huang , Yan-Gang Sun , Shui-Bing Liu , Yun-Qing Li
{"title":"丘脑束旁核向岛叶皮质的投射介导小鼠的镇痛和抗焦虑行为。","authors":"Fei Li , Zi-Ang Li , Jia Li , Hui-Min Tian , Dong-Ning Li , Zhong-Yi Liu , Jin Cheng , Tian-Yu Zhao , Li-Ming Liu , Yao-Hua Liu , Sha-Sha Tao , Fen-Sheng Huang , Yan-Gang Sun , Shui-Bing Liu , Yun-Qing Li","doi":"10.1016/j.nbd.2025.107107","DOIUrl":null,"url":null,"abstract":"<div><div>The parafascicular nucleus of the thalamus (PF), part of the intralaminar nuclei of the thalamus, plays critical roles in both motor and pain regulations. In this study, the projection from the ventral region of the PF to the dorsal area of the insular cortex (IC) were identified using a neuroanatomical approach. Then, chemogenetic inhibition or activation of the PF-IC neural pathway in the normal mice or in the spared nerve injury (SNI) model mice induced hyperalgesia and anxiety-like behaviors or alleviated hypersensitivity and anxiety-like behaviors, respectively. Additionally, a reduction in the intrinsic electrophysiological activity of the PF neurons projecting to the IC was recorded in 2-week SNI mice. Finally, the results of viral tracing and immunofluorescence histochemical staining demonstrated that the fibers and terminals projecting from the PF predominantly terminated on the parvalbumin-positive interneurons. These findings suggest that the activity of the PF-IC neuronal pathway is suppressed under neuropathic pain condition and that the activation of this pathway exhibits analgesic and anxiolytic effects in mice suffering from nerve injury.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"216 ","pages":"Article 107107"},"PeriodicalIF":5.6000,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Projection from the parafascicular nucleus of the thalamus to the insular cortex mediate analgesia and anti-anxiety behaviors in mice\",\"authors\":\"Fei Li , Zi-Ang Li , Jia Li , Hui-Min Tian , Dong-Ning Li , Zhong-Yi Liu , Jin Cheng , Tian-Yu Zhao , Li-Ming Liu , Yao-Hua Liu , Sha-Sha Tao , Fen-Sheng Huang , Yan-Gang Sun , Shui-Bing Liu , Yun-Qing Li\",\"doi\":\"10.1016/j.nbd.2025.107107\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>The parafascicular nucleus of the thalamus (PF), part of the intralaminar nuclei of the thalamus, plays critical roles in both motor and pain regulations. In this study, the projection from the ventral region of the PF to the dorsal area of the insular cortex (IC) were identified using a neuroanatomical approach. Then, chemogenetic inhibition or activation of the PF-IC neural pathway in the normal mice or in the spared nerve injury (SNI) model mice induced hyperalgesia and anxiety-like behaviors or alleviated hypersensitivity and anxiety-like behaviors, respectively. Additionally, a reduction in the intrinsic electrophysiological activity of the PF neurons projecting to the IC was recorded in 2-week SNI mice. Finally, the results of viral tracing and immunofluorescence histochemical staining demonstrated that the fibers and terminals projecting from the PF predominantly terminated on the parvalbumin-positive interneurons. These findings suggest that the activity of the PF-IC neuronal pathway is suppressed under neuropathic pain condition and that the activation of this pathway exhibits analgesic and anxiolytic effects in mice suffering from nerve injury.</div></div>\",\"PeriodicalId\":19097,\"journal\":{\"name\":\"Neurobiology of Disease\",\"volume\":\"216 \",\"pages\":\"Article 107107\"},\"PeriodicalIF\":5.6000,\"publicationDate\":\"2025-09-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurobiology of Disease\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0969996125003249\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurobiology of Disease","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0969996125003249","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Projection from the parafascicular nucleus of the thalamus to the insular cortex mediate analgesia and anti-anxiety behaviors in mice
The parafascicular nucleus of the thalamus (PF), part of the intralaminar nuclei of the thalamus, plays critical roles in both motor and pain regulations. In this study, the projection from the ventral region of the PF to the dorsal area of the insular cortex (IC) were identified using a neuroanatomical approach. Then, chemogenetic inhibition or activation of the PF-IC neural pathway in the normal mice or in the spared nerve injury (SNI) model mice induced hyperalgesia and anxiety-like behaviors or alleviated hypersensitivity and anxiety-like behaviors, respectively. Additionally, a reduction in the intrinsic electrophysiological activity of the PF neurons projecting to the IC was recorded in 2-week SNI mice. Finally, the results of viral tracing and immunofluorescence histochemical staining demonstrated that the fibers and terminals projecting from the PF predominantly terminated on the parvalbumin-positive interneurons. These findings suggest that the activity of the PF-IC neuronal pathway is suppressed under neuropathic pain condition and that the activation of this pathway exhibits analgesic and anxiolytic effects in mice suffering from nerve injury.
期刊介绍:
Neurobiology of Disease is a major international journal at the interface between basic and clinical neuroscience. The journal provides a forum for the publication of top quality research papers on: molecular and cellular definitions of disease mechanisms, the neural systems and underpinning behavioral disorders, the genetics of inherited neurological and psychiatric diseases, nervous system aging, and findings relevant to the development of new therapies.