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Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats.
Mol Brain. 2019 09 04; 12(1):76.MB

Abstract

Central sensitization plays a pivotal role in the maintenance of chronic pain induced by chronic pancreatitis (CP), but cortical modulation of painful CP remains elusive. This study was designed to examine the role of anterior insular cortex (aIC) in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced by intraductal administration of trinitrobenzene sulfonic acid (TNBS). Abdomen hyperalgesia and anxiety were assessed by von Frey filament and open field tests, respectively. Two weeks after surgery, the activation of aIC was indicated by FOS immunohistochemical staining and electrophysiological recordings. Expressions of VGluT1, NMDAR subunit NR2B and AMPAR subunit GluR1 were analyzed by immunoblottings. The regulatory roles of aIC in hyperalgesia and pain-related anxiety were detected via pharmacological approach and chemogenetics in CP rats. Our results showed that TNBS treatment resulted in long-term hyperalgesia and anxiety-like behavior in rats. CP rats exhibited increased FOS expression and potentiated excitatory synaptic transmission within aIC. CP rats also showed up-regulated expression of VGluT1, and increased membrane trafficking and phosphorylation of NR2B and GluR1 within aIC. Blocking excitatory synaptic transmission significantly attenuated abdomen mechanical hyperalgesia. Specifically inhibiting the excitability of insular pyramidal cells reduced both abdomen hyperalgesia and pain-related anxiety. In conclusion, our findings emphasize a key role for aIC in hyperalgesia and anxiety of painful CP, providing a novel insight into cortical modulation of painful CP and shedding light on aIC as a potential target for neuromodulation interventions in the treatment of CP.

Authors+Show Affiliations

Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Department of Gastroenterology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710032, China.Department of Anatomy, Fujian Medical University, Fuzhou, 350108, China.Department of Anatomy, Guangxi Medical University, Nanning, 530021, China.Department of Anatomy, Fujian Health College, Fuzhou, 350101, China.Department of Cardiology, The Second Affiliated Hospital of Xian Jiaotong University, Xian Jiaotong University, Xi'an, 710004, China.Department of Cardiology, The Second Affiliated Hospital of Xian Jiaotong University, Xian Jiaotong University, Xi'an, 710004, China.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Joint Laboratory of Neuroscience at Hainan Medical University and Fourth Military Medical University, Hainan Medical University, Haikou, 571199, China.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China.Department of Cardiology, The Second Affiliated Hospital of Xian Jiaotong University, Xian Jiaotong University, Xi'an, 710004, China. 277399335@qq.com.Department of Anatomy, Histology and Embryology & K. K. Leung Brain Research Centre, Fourth Military Medical University, No. 169, West Chang-le Road, Xi'an, 710032, China. deptanat@fmmu.edu.cn. Joint Laboratory of Neuroscience at Hainan Medical University and Fourth Military Medical University, Hainan Medical University, Haikou, 571199, China. deptanat@fmmu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

31484535

Citation

Bai, Yang, et al. "Anterior Insular Cortex Mediates Hyperalgesia Induced By Chronic Pancreatitis in Rats." Molecular Brain, vol. 12, no. 1, 2019, p. 76.
Bai Y, Ma LT, Chen YB, et al. Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats. Mol Brain. 2019;12(1):76.
Bai, Y., Ma, L. T., Chen, Y. B., Ren, D., Chen, Y. B., Li, Y. Q., Sun, H. K., Qiu, X. T., Zhang, T., Zhang, M. M., Yi, X. N., Chen, T., Li, H., Fan, B. Y., & Li, Y. Q. (2019). Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats. Molecular Brain, 12(1), 76. https://doi.org/10.1186/s13041-019-0497-5
Bai Y, et al. Anterior Insular Cortex Mediates Hyperalgesia Induced By Chronic Pancreatitis in Rats. Mol Brain. 2019 09 4;12(1):76. PubMed PMID: 31484535.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats. AU - Bai,Yang, AU - Ma,Li-Tian, AU - Chen,Yan-Bing, AU - Ren,Dan, AU - Chen,Ying-Biao, AU - Li,Ying-Qi, AU - Sun,Hong-Ke, AU - Qiu,Xin-Tong, AU - Zhang,Ting, AU - Zhang,Ming-Ming, AU - Yi,Xi-Nan, AU - Chen,Tao, AU - Li,Hui, AU - Fan,Bo-Yuan, AU - Li,Yun-Qing, Y1 - 2019/09/04/ PY - 2019/06/30/received PY - 2019/08/23/accepted PY - 2019/9/6/entrez PY - 2019/9/6/pubmed PY - 2020/6/2/medline KW - Anterior insular cortex KW - Anxiety KW - Chronic pancreatitis KW - Excitatory synaptic transmission KW - Hyperalgesia KW - Long-term potentiation KW - Rat SP - 76 EP - 76 JF - Molecular brain JO - Mol Brain VL - 12 IS - 1 N2 - Central sensitization plays a pivotal role in the maintenance of chronic pain induced by chronic pancreatitis (CP), but cortical modulation of painful CP remains elusive. This study was designed to examine the role of anterior insular cortex (aIC) in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced by intraductal administration of trinitrobenzene sulfonic acid (TNBS). Abdomen hyperalgesia and anxiety were assessed by von Frey filament and open field tests, respectively. Two weeks after surgery, the activation of aIC was indicated by FOS immunohistochemical staining and electrophysiological recordings. Expressions of VGluT1, NMDAR subunit NR2B and AMPAR subunit GluR1 were analyzed by immunoblottings. The regulatory roles of aIC in hyperalgesia and pain-related anxiety were detected via pharmacological approach and chemogenetics in CP rats. Our results showed that TNBS treatment resulted in long-term hyperalgesia and anxiety-like behavior in rats. CP rats exhibited increased FOS expression and potentiated excitatory synaptic transmission within aIC. CP rats also showed up-regulated expression of VGluT1, and increased membrane trafficking and phosphorylation of NR2B and GluR1 within aIC. Blocking excitatory synaptic transmission significantly attenuated abdomen mechanical hyperalgesia. Specifically inhibiting the excitability of insular pyramidal cells reduced both abdomen hyperalgesia and pain-related anxiety. In conclusion, our findings emphasize a key role for aIC in hyperalgesia and anxiety of painful CP, providing a novel insight into cortical modulation of painful CP and shedding light on aIC as a potential target for neuromodulation interventions in the treatment of CP. SN - 1756-6606 UR - https://www.unboundmedicine.com/medline/citation/31484535/Anterior_insular_cortex_mediates_hyperalgesia_induced_by_chronic_pancreatitis_in_rats_ L2 - https://molecularbrain.biomedcentral.com/articles/10.1186/s13041-019-0497-5 DB - PRIME DP - Unbound Medicine ER -