Low-Intensity Focused Ultrasound Alleviates Chronic Neuropathic Pain-Induced Allodynia by Inhibiting Neuroplasticity in the Anterior Cingulate Cortex.
Low-Intensity Focused Ultrasound Alleviates Chronic Neuropathic Pain-Induced Allodynia by Inhibiting Neuroplasticity in the Anterior Cingulate Cortex.
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DOI：
10.1155/2022/6472475
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发表时间：
2022
影响因子：
3.1
通讯作者：
Ao, Li-Juan
中科院分区：
文献类型：
--
作者：
Wang, Bin;Chen, Mo-Xian;Chen, Shao-Chun;Feng, Xiang-Jun;Liao, Ye-Hui;Zhao, Yun-Xin;Tie, Jin-Shan;Liu, Yao;Ao, Li-Juan
低强度聚焦超声（LIFU）是一种通过调节中枢神经系统来缓解异常性疼痛的潜在无创方法。然而，潜在的镇痛机制仍未被探索。在这里，我们评估了前扣带皮层（ACC）的LIFU如何影响慢性收缩性损伤（CCI）导致的行为反应和中枢可塑性。采用苏木精伊红（H&E）染色和氟玉C （FJC）染色评价LIFU刺激的安全性。小鼠CCI术后第91天开始进行21天超声暴露治疗。我们使用Von Frey细丝（VFFs）评估50%机械退出阈值（MWT50）。通过western blotting （WB）和免疫荧光（IF）染色检测ACC组织中微管相关蛋白2 （MAP2）、生长相关蛋白43 （GAP43）和tau蛋白的表达水平，评价ACC组织的中枢可塑性。LIFU刺激可有效、安全地激活ACC区域，显著增加c-fos阳性细胞数量（P < 0.05），无出血、凝固性坏死和神经元丢失。慢性神经性疼痛（CNP-）诱导的异常性疼痛时，MWT50显著降低（P < 0.05）， MAP2、GAP43、tau蛋白也过表达。治疗3周后，CCI+LIFU组MWT50较CCI组显著升高（P < 0.05）。WB和IF染色均显示MAP2、GAP43和tau的表达水平显著降低（P < 0.05）。LIFU治疗ACC可有效减弱cnp诱发的疼痛机械敏感性，逆转中枢可塑性异常。
Low-intensity focused ultrasound (LIFU) is a potential noninvasive method to alleviate allodynia by modulating the central nervous system. However, the underlying analgesic mechanisms remain unexplored. Here, we assessed how LIFU at the anterior cingulate cortex (ACC) affects behavior response and central plasticity resulting from chronic constrictive injury (CCI). The safety of LIFU stimulation was assessed by hematoxylin and eosin (H&E) and Fluoro-Jade C (FJC) staining. A 21-day ultrasound exposure therapy was conducted from day 91 after CCI surgery in mice. We assessed the 50% mechanical withdrawal threshold (MWT50) using Von Frey filaments (VFFs). The expression levels of microtubule-associated protein 2 (MAP2), growth-associated protein 43 (GAP43), and tau were determined via western blotting (WB) and immunofluorescence (IF) staining to evaluate the central plasticity in ACC. The regions of ACC were activated effectively and safely by LIFU stimulation, which significantly increased the number of c-fos-positive cells (P < 0.05) with no bleeding, coagulative necrosis, and neuronal loss. Under chronic neuropathic pain- (CNP-) induced allodynia, MWT50 decreased significantly (P < 0.05), and overexpression of MAP2, GAP43, and tau was also observed. After 3 weeks of treatment, significant increases in MWT50 were found in the CCI+LIFU group compared with the CCI group (P < 0.05). WB and IF staining both demonstrated a significant reduction in the expression levels of MAP2, GAP43, and tau (P < 0.05). LIFU treatment on ACC can effectively attenuate CNP-evoked mechanical sensitivity to pain and reverse aberrant central plasticity.
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影响因子：
5.1
作者：
Kuffler, Damien P.
通讯作者：
Kuffler, Damien P.
影响因子：
158.5
作者：
Martinez-Fernandez, Raul;Manez-Miro, Jorge U.;Obeso, Jose A.
通讯作者：
Obeso, Jose A.
影响因子：
3.3
作者：
Lu JS;Chen QY;Chen X;Li XH;Zhou Z;Liu Q;Lin Y;Zhou M;Xu PY;Zhuo M
通讯作者：
Zhuo M
影响因子：
16.2
作者：
Folloni, Davide;Verhagen, Lennart;Sallet, Jerome
通讯作者：
Sallet, Jerome
影响因子：
10.6
作者：
Barthas, Florent;Humo, Muris;Yalcin, Ipek
通讯作者：
Yalcin, Ipek