• Acta Pharmacol. Sin. · Dec 2006

    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.

    • Xian-jie Wen, Zhang-jun Li, Zhi-xin Chen, Zhi-yuan Fang, Chen-xiang Yang, Heng Li, and Yin-ming Zeng.
    • Department of Anesthesiology, the First Peopleos Hospital of FoShan and Affiliated FoShan Hospital of Sun-Yat Sen University, Foshan 528000, China.
    • Acta Pharmacol. Sin. 2006 Dec 1;27(12):1547-52.

    AimThe 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.MethodsThe 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.ResultsCCD 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.ConclusionCav3.2 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.

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