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Central Sensitization-Related Changes in Brain Function Activity in a Rat Endometriosis-Associated Pain Model

Authors Zheng P, Jia S, Guo D, Chen S, Zhang W, Cheng A, Xie W, Sun G, Leng J, Lang J

Received 24 September 2019

Accepted for publication 17 December 2019

Published 13 January 2020 Volume 2020:13 Pages 95—107


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Michael A Überall

Ping Zheng, 1 Shuangzheng Jia, 1 Dalong Guo, 2 Sikai Chen, 1 Wen Zhang, 1 Aoshuang Cheng, 1 Weijie Xie, 3 Guibo Sun, 3 Jinhua Leng, 1 Jinghe Lang 1

1Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, People’s Republic of China; 2Air Force Medical Center, PLA, Beijing, People’s Republic of China; 3Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, People’s Republic of China

Correspondence: Jinghe Lang Email
Jinhua Leng Email

Background: Pain sensitization processing in the central nervous system may be related to endometriosis-associated pain in patients. The purpose of this study was to understand the alterations in the abnormal pain response in central brain areas and explore the central sensitization mechanism of endometriosis-associated pain.
Methods: An endometriosis model was established in 40 Sprague-Dawley rats, and the rats underwent pain model assessment through behavioral tests. Twenty Sprague-Dawley rats underwent a sham operation as the control group. Thirteen pain rats and 8 control rats received Rs-fMRI examination to explore the brain functional activity areas, and the regional homogeneity (ReHo) method was used to analyze relevant functional signals among the whole brain. The states of neurons and expression of TRPV1 and NMDRA located in the abnormal ReHo signal brain regions were observed using Nissl staining, qRT-PCR and immunohistochemistry.
Results: The rats were divided into a pain group and a control group based on the different syndromes and behavioral assessments. We detected significant enhancement of ReHo signals in the anterior cingulate cortex, hippocampus, and thalamus and a reduction in the ReHo values in the basomedial amygdaloid nucleus (BM) and primary motor cortex (M1) in the pain rat group via Rs-fMRI examination. The number of Nissl bodies and apoptotic neurons was increased; moreover, the volume of neurons increased compensatorily in the cingulate cortex, thalamus and hippocampus in the pain group. TRPV1 and NMDRA were overexpressed in apoptotic neurons in the higher ReHo value brain regions in the endometriosis pain group.
Conclusion: These findings suggest that in rats with endometriosis-associated pain, ReHo signal enhancement was observed in the cingulate cortex, thalamus and hippocampus, which may be due to the increase in the number of apoptotic neurons or the compensatory increase in the volume of overactive neurons.

Keywords: endometriosis-associated pain, rat model, behavioral assessment, central sensitization, Rs-fMRI, regional homogeneity, TRPV1, NMDRA

Corrigendum for this paper has been published

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