论文部分内容阅读
目的观察鞘内注射Cav3.3反义寡聚核苷酸对慢性背根节压迫(chronic compression of dorsal root ganglion,CCD)大鼠痛阈的影响,探讨脊髓Cav3.3T型钙通道在神经病理痛中的作用。方法鞘内置管的雄性SD大鼠32只,随机分为4组(行为学n=8,):CCD+NS组、CCD+Cav3.3反义核苷酸组(CCD+Cav3.3-AS)、CCD+Cav3.3错义核苷酸组(CCD+Cav3.3-MM)、假手术(sham)+NS组。各组大鼠在CCD或sham后第1天开始连续4d每天两次鞘内分别注射Cav3.3-AS、Cav3.3-MM12.5μg/10μl或NS10μl,行为学部分分别观察术后1、3、5、7、10、14d大鼠机械缩足阈值(mechanica lwithdrawal threshold,MWT)和热缩足潜伏期(thermal withdrawal latency,TWL)。结果鞘内注射Cav3.3反义寡聚核苷酸能显著延缓CCD大鼠痛敏的形成,在CCD术后10d才形成与CCD+NS组类似的痛敏,而鞘内注射Cav3.3错义核苷酸则与NS组无统计学差异。结论脊髓Cav3.3参与神经病理痛的形成,抑制脊髓Cav3.3基因的表达具有疼痛治疗作用。
Objective To observe the effect of intrathecal injection of Cav3.3 antisense oligonucleotide on the pain threshold in chronic compression of dorsal root ganglion (CCD) rats and to explore the effect of Cav3.3T-type calcium channel in neuropathic pain In the role. Methods Thirty-two male SD rats were randomly divided into 4 groups (behavioral n = 8): CCD + NS group, CCD + Cav3.3 antisense nucleotide group (CCD + Cav3.3-AS ), CCD + Cav3.3 missense nucleotide group (CCD + Cav3.3-MM), sham + NS group. Rats in each group were injected with Cav3.3-AS, Cav3.3-MM12.5μg / 10μl or NS10μl intrathecally twice a day for 4 days continuously on the first day after CCD or sham. , Mechanic l withdrawal threshold (MWT) and thermal withdrawal latency (TWL) on 5, 7, 10 and 14 days. Results intrathecal injection of Cav3.3 antisense oligonucleotides can significantly delay the formation of hyperalgesia in CCD rats, forming a pain sensation similar to CCD + NS group 10 days after the operation of the CCD, while intrathecal Cav3.3 injection There was no significant difference between the sense nucleotides and the NS group. Conclusion Cav3.3 is involved in the formation of neuropathic pain and inhibits the expression of Cav3.3 gene in spinal cord.