title: Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury.
abstract: Autophagy is a process of cellular self-cannibalization, and provides an adaptive mechanism to protect cells against diverse pathological settings. Following peripheral nerve injury, autophagic process was changed in Schwann cells and spinal neurons and glial cells, implicating a vital role of autophagy in chronic pain. However, little is known about the role of autophagy in dorsal root ganglion (DRG) in neuropathic pain. In the present study, we investigated the autophagic process in DRG and its effect on neuropathic pain induced by L5 spinal nerve ligation (SNL). The level of microtubule associated protein 1 light chain 3 (LC3)-II, a general marker for autophagy, was increased in L5 DRG after SNL. Immunofluorescence staining showed that LC3-II puncta were observed in DRG neurons after SNL. Injection of autophagy inducer rapamycin into L5 DRG before or after SNL dose-dependently attenuated neuropathic pain. The expression of LC3 was enhanced in L5 DRG by rapamycin. These data suggest that the autophagy in L5 DRG neurons is a defensive reaction to L5 spinal nerve injury, and pharmacological enhancement of autophagy may be a potential treatment to prevent the onset and chronification of neuropathic pain.
authors.affiliation: Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China; Co-innovative Center of Neuroregenaration, Nantong University, Nantong 226001, China.
authors.forename: Jian-Shuang
authors.initials: JS
authors.lastname: Guo
authors.affiliation: Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China.
authors.forename: Peng-Bo
authors.initials: PB
authors.lastname: Jing
authors.affiliation: Department of Anatomy, Medical School of Nantong University, Nantong 226001, China.
authors.forename: Ji-An
authors.initials: JA
authors.lastname: Wang
authors.affiliation: Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhang
authors.affiliation: Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China.
authors.forename: Bao-Chun
authors.initials: BC
authors.lastname: Jiang
authors.affiliation: Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong 226001, China; Co-innovative Center of Neuroregenaration, Nantong University, Nantong 226001, China.
authors.forename: Yong-Jing
authors.initials: YJ
authors.lastname: Gao
authors.affiliation: Department of Anatomy, Medical School of Nantong University, Nantong 226001, China; Co-innovative Center of Neuroregenaration, Nantong University, Nantong 226001, China. Electronic address: zhangzhijun6042@163.com.
authors.forename: Zhi-Jun
authors.initials: ZJ
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001343:Autophagy; D005727:Ganglia, Spinal / Q000473:pathology*; D006930:Hyperalgesia / Q000503:physiopathology; D008813:Mice, Inbred ICR; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009437:Neuralgia / Q000473:pathology / Q000503:physiopathology*; D010812:Physical Stimulation; D013127:Spinal Nerves / Q000293:injuries / Q000473:pathology / Q000503:physiopathology*
chemical_list: C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins
keywords: Autophagy; Dorsal root ganglion; Neuropathic pain; Rapamycin; Spinal nerve ligation