中文摘要：

背景 Cav3.2是T型钙通道的一种亚型,在脊髓背根神经节中分布广泛.研究表明：低电压激活的T型钙离子（Ca2＋）通道参与神经病理痛的形成.Car3.2在慢性疼痛,尤其是在化疗药紫杉醇诱发的痛觉过敏中的作用已成为研究关注的热点.目的 阐明T型钙通道Cav3.2在紫杉醇诱发神经痛觉过敏中的作用.内容 就Car3.2的电生理特性、参与疼痛的可能机制、与不同疼痛间的关系等方面进行阐述.趋向 T型钙通道Cav3.2亚型在痛觉过敏的发生发展过程中发挥着重要作用.充分了解Cav3.2的生理作用,阐明其参与紫杉醇诱发的痛觉过敏的可能机制,可为化疗药所致痛觉过敏的防治提供思路.

英文摘要：

Background As a subtype of T-type calcium channels,Cav3.2 is widely distributed in the spinal cord and dorsal root ganglia.Previous studies have shown that low voltage activation of T-type calcium channel may be involved in the pathogenesis of neural pathological pain.The role of Cav3.2 in chronic pain,especially pathogenesis of paclitaxel-induced pain hypersensitivity has increasingly become a research hotspot.Objective This review is to sum the mechanism of modulation of Cav3.2 in paclitaxel-induced hyperalgesia.Content The review includes the electrophysiological properties of Cav3.2,the feasible mechanisms involved in pain,and the relationship between different aspects of pain.Trend As a subtype of T-type calcium channels,Cav3.2 plays a critical role in the process of development of hyperalgesia.It is important for the treatment strategy of the chemotherapy-evoked neuropathic pain to clarify the physiological role of Cav3.2 and its role in the pathogenesis in paclitaxel-induced hyperalgesia.