鞘内注射Cav3.2和Cav3.3反义寡核苷酸可逆转大鼠背根神经节慢性压迫后出现的触觉异常性疼痛和热痛觉过敏。
Intrathecal administration of Cav3.2 and Cav3.3 antisense oligonucleotide reverses tactile allodynia and thermal hyperalgesia in rats following chronic compression of dorsal root of ganglion.
作者信息
Wen Xian-jie, Li Zhang-jun, Chen Zhi-xin, Fang Zhi-yuan, Yang Chen-xiang, Li Heng, Zeng Yin-ming
机构信息
Department of Anesthesiology, the First Peopleos Hospital of FoShan and Affiliated FoShan Hospital of Sun-Yat Sen University, Foshan 528000, China.
出版信息
Acta Pharmacol Sin. 2006 Dec;27(12):1547-52. doi: 10.1111/j.1745-7254.2006.00461.x.
AIM
The present study aimed to elucidate the role of T-subtype calcium channels (Cav3.1, Cav3.2, and Cav3.3) in the pathogenesis of neuropathic pain at spinal level.
METHODS
The chronic compression of the dorsal root ganglion (CCD) rat model was adopted. The antisense oligonucleotide of Cav3.1, Cav3.2, and Cav3.3 or normal saline (NS) were intrathecally administered twice per day from the first day to the fourth day after operation. Paw mechanical withdrawal threshold and paw thermal withdrawal latency were measured to evaluate the tactile allodynia and thermal hyperalgesia, respectively.
RESULTS
CCD rats developed reliable tactile allodynia and thermal hyperalgesia after operation. Intrathecal administration of antisense oligonucleotide of Cav3.2 and Cav3.3 significantly relieved tactile allodynia and thermal hyperalgesia in CCD rats, but not Cav3.1.
CONCLUSION
Cav3.2 and Cav3.3 subtype calcium channels in the spinal cord may play an important role in the pathogenesis of neuropathic pain, which may contribute to the management of the neuropathic pain.
目的
本研究旨在阐明T型钙通道（Cav3.1、Cav3.2和Cav3.3）在脊髓水平神经性疼痛发病机制中的作用。
方法
采用背根神经节慢性压迫（CCD）大鼠模型。术后第1天至第4天，每天两次鞘内注射Cav3.1、Cav3.2和Cav3.3的反义寡核苷酸或生理盐水（NS）。分别测量爪部机械性缩足阈值和爪部热缩足潜伏期，以评估触觉异常性疼痛和热痛觉过敏。
结果
CCD大鼠术后出现可靠的触觉异常性疼痛和热痛觉过敏。鞘内注射Cav3.2和Cav3.3的反义寡核苷酸可显著缓解CCD大鼠的触觉异常性疼痛和热痛觉过敏，但Cav3.1的反义寡核苷酸无此作用。
结论
脊髓中的Cav3.2和Cav3.3亚型钙通道可能在神经性疼痛的发病机制中起重要作用，这可能有助于神经性疼痛的治疗。
Zotero 插件