Microglial Depletion does not Affect the Laterality of Mechanical Allodynia in Mice.
10.1007/s12264-022-01017-2
- Author:
Quan MA
1
;
Dongmei SU
2
;
Jiantao HUO
2
;
Guangjuan YIN
2
;
Dong DONG
2
;
Kaifang DUAN
2
;
Hong CHENG
2
;
Huiling XU
3
;
Jiao MA
3
;
Dong LIU
2
;
Bin MOU
4
;
Jiyun PENG
5
;
Longzhen CHENG
6
Author Information
1. School of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
2. Shenzhen Key Laboratory of Gene Regulation and Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
3. Department of Biology, Brain Research Center, Southern University of Science and Technology, Shenzhen, 518055, China.
4. Institute of Life Science, Nanchang University, Nanchang, 330031, China.
5. Institute of Life Science, Nanchang University, Nanchang, 330031, China. pengjy@ncu.edu.cn.
6. Shenzhen Key Laboratory of Gene Regulation and Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China. chenglz@sustech.edu.cn.
- Publication Type:Journal Article
- Keywords:
Aβ;
Dynamic allodynia;
Laterality;
Mechanical allodynia;
Microglia;
Punctate allodynia;
Spinal dorsal horn
- MeSH:
Mice;
Animals;
Hyperalgesia/metabolism*;
Microglia/metabolism*;
Disease Models, Animal;
Spinal Cord/metabolism*;
Spinal Cord Dorsal Horn/metabolism*;
Ganglia, Spinal/metabolism*
- From:
Neuroscience Bulletin
2023;39(8):1229-1245
- CountryChina
- Language:English
-
Abstract:
Mechanical allodynia (MA), including punctate and dynamic forms, is a common and debilitating symptom suffered by millions of chronic pain patients. Some peripheral injuries result in the development of bilateral MA, while most injuries usually led to unilateral MA. To date, the control of such laterality remains poorly understood. Here, to study the role of microglia in the control of MA laterality, we used genetic strategies to deplete microglia and tested both dynamic and punctate forms of MA in mice. Surprisingly, the depletion of central microglia did not prevent the induction of bilateral dynamic and punctate MA. Moreover, in dorsal root ganglion-dorsal root-sagittal spinal cord slice preparations we recorded the low-threshold Aβ-fiber stimulation-evoked inputs and outputs of superficial dorsal horn neurons. Consistent with behavioral results, microglial depletion did not prevent the opening of bilateral gates for Aβ pathways in the superficial dorsal horn. This study challenges the role of microglia in the control of MA laterality in mice. Future studies are needed to further understand whether the role of microglia in the control of MA laterality is etiology-or species-specific.
