scholarly journals Microglia Are Indispensable for Synaptic Plasticity in the Spinal Dorsal Horn and Chronic Pain

Cell Reports ◽  
2019 ◽  
Vol 27 (13) ◽  
pp. 3844-3859.e6 ◽  
Author(s):  
Li-Jun Zhou ◽  
Jiyun Peng ◽  
Ya-Nan Xu ◽  
Wei-Jie Zeng ◽  
Jun Zhang ◽  
...  
Pain ◽  
2019 ◽  
Vol 160 (5) ◽  
pp. 1082-1092 ◽  
Author(s):  
Zongqin Zhang ◽  
Xiaobao Ding ◽  
Zhiwei Zhou ◽  
Zhuang Qiu ◽  
Naihao Shi ◽  
...  

Neuroscience ◽  
1997 ◽  
Vol 82 (2) ◽  
pp. 559-574 ◽  
Author(s):  
J.R Goff ◽  
A.R Burkey ◽  
D.J Goff ◽  
L Jasmin

2021 ◽  
Author(s):  
Xianqiao Xie ◽  
Yang Li ◽  
Shanchun Su ◽  
Xiaohui Li ◽  
Xueqin Xu ◽  
...  

Abstract Background The underlying mechanism of chronic pain involves the plasticity in synaptic receptors and neurotransmitters. This study aimed to investigate potential roles of neuroligins (NLs) within the spinal dorsal horn of rats in a newly established bone cancer pain (BCP) model. Methods Using our rat BCP model, we assessed pain hypersensitivity over time. Quantitative real-time polymerase chain reaction and Western blot analysis were performed to investigate NL expression, and NLs were overexpressed in the rat spinal cord using lentiviral vectors. Immunofluorescence staining and whole-cell patch-clamp recordings were deployed to investigate the role of NLs in the development of BCP. Results We observed reduced expression levels of NL1 and NL2, but not NL3, within the rat spinal cord, which were found to be associated with and essential for the development of BCP in our model. Accordingly, NL1 or NL2 overexpression in the spinal cord alleviated mechanical hypersensitivity of rats. Electrophysiological experiments indicated that NL1 and NL2 are involved in BCP via regulating γ-aminobutyric acid-ergic interneuronal synapses and the activity of glutamatergic interneuronal synapses, respectively. Conclusions Our observations unravel the role of NLs in cancer-related chronic pain and further suggest that inhibitory mechanisms are central features of BCP in the spinal dorsal horn. These results provide a new perspective and basis for subsequent studies elucidating the onset and progression of BCP.


2007 ◽  
Vol 208 (2) ◽  
pp. 323-332 ◽  
Author(s):  
Guo-Gang Xing ◽  
Feng-Yu Liu ◽  
Xiao-Xiu Qu ◽  
Ji-Sheng Han ◽  
You Wan

2021 ◽  
pp. 096452842110207
Author(s):  
Ying Jin ◽  
Jie Zhou ◽  
Fangfang Xu ◽  
Zeqin Ren ◽  
Jun Hu ◽  
...  

Background: Hyperalgesic priming (HP) is a model of the transition from acute to chronic pain. Electroacupuncture (EA) could inhibit pain development through the peripheral dorsal root ganglia; however, it is unclear whether it can mitigate the transition from acute to chronic pain by attenuating protein expression in the p38 MAPK (mitogen-activated protein kinase)/tumour necrosis factor alpha (TNF-α) pathway in the spinal dorsal horn. Aims: We aimed to determine whether EA could prevent the transition from acute to chronic pain by affecting the p38 MAPK/TNF-α pathway in the spinal dorsal horn in a rat model established using HP. Methods: We first randomly subdivided 30 male Sprague-Dawley (SD) rats into 5 groups ( n = 6 per group): control (N), sham HP (Sham-HP), HP, HP + SB203580p38 MAPK (HP+SB203580), and HP + Lenalidomide (CC-5013) (HP+Lenalidomide). We then randomly subdivided a further 30 male SD rats into 5 groups ( n = 6 per group): Sham-HP, HP, sham EA (Sham EA), EA (EA), and EA + U-46619 p38 MAPK agonist (EA+U-46619). We assessed the effects of EA on the mechanical paw withdrawal threshold and p38 MAPK/TNF-α expression in the spinal dorsal horn of rats subjected to chronic inflammatory pain. Results: Rats in the EA group had reduced p38 MAPK and TNF-α expression and had significantly reduced mechanical hyperalgesia compared with rats in the other groups. Conclusion: Our findings indicate that EA could increase the mechanical pain threshold in rats and inhibit the transition from acute pain to chronic pain. This mechanism could involve reduced p38 MAPK/TNF-α expression in the spinal dorsal horn.


2009 ◽  
Vol 64 (2) ◽  
pp. 133-136 ◽  
Author(s):  
Hiroshi Ikeda ◽  
Takaki Kiritoshi ◽  
Kazuyuki Murase

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