Loss of ICA69 Potentiates Long-Lasting Hyperalgesia After Subcutaneous Formalin Injection into the Mouse Hindpaw
| Autor: | Ya-Wen Zhang, Na-Na Li, Bin-Yu Chen, Zhen Wang, Jun-Lu Wang, Dan-Yun Jia, Ying Shen, Yong-Xing Yao, Ya-Nan Wang, Qian-Jun Li, Shen-Hui Jin, Meizi Qian |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Time Factors Injections Subcutaneous media_common.quotation_subject AMPA receptor Pharmacology Autoantigens Biochemistry Mice Cellular and Molecular Neuroscience Formaldehyde medicine Animals Internalization media_common Mice Knockout Microglia business.industry General Medicine Spinal cord Hindlimb Mice Inbred C57BL medicine.anatomical_structure Hyperalgesia Immunology Knockout mouse Phosphorylation medicine.symptom PICK1 business |
| Zdroj: | Neurochemical Research. 40:579-590 |
| ISSN: | 1573-6903 0364-3190 |
| DOI: | 10.1007/s11064-014-1503-z |
| Popis: | Islet-cell autoantigen 69 kDa (ICA69) plays an important role in many diseases and physiological activities by forming heteromeric complexes with protein interacts with C-kinase 1 (PICK1). PICK1 is critical for inflammatory pain hypersensitivity by regulating trafficking of AMPA receptor subunit GluA2 in spinal neurons. However, the role of ICA69 in inflammatory pain has not yet been investigated. Here we reported that expression of PICK1 in spinal cord was reduced largely in ICA69 knockout mice. The pain hypersensitivity was enhanced in the second phase 7 days after formalin administration. Meanwhile, increased Ser880 phosphorylation in GluA2 and decreased surface GluA2 were concordant with the pain. Furthermore, the number of activated microglia in spinal dorsal horn increased in line with pain hypersensitivity. Together, ICA69 deficiency promoted the internalization of GluA2 and FML-induced long-lasting pain hypersensitivity. In addition, microglia activation might be an important factor in the development of the pain hypersensitivity. |
| Databáze: | OpenAIRE |
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