【摘要】 伤害性感受器激活引起疼痛的概念,现已广泛被人们接受。大量实验表明,伤害性感受器兴奋性的变化与一些离子通道有关。对河豚毒素不敏感的电压依赖性钠离子通道（TTXr）选择性地分布于与伤害性感受有关的初级感受神经元。炎症反应和神经损伤诱发的慢性疼痛可诱发这种TTXr功能及基因表达的变化。TTXr通道蛋白的反义寡核苷酸（antisense ODN）处理可对抗炎症或神经损伤引起的痛觉过敏或超敏。提示TTXr在伤害性感受中起重要作用,有望成为特异性镇痛药物的药理作用靶点。更多还原

【Abstract】 It has been generaly accepted that the activation of nociceptors leads to the sensation of pain. Many experiments show that changes of nociceptors sensitivity are related to some ion channels. The voltage-dependent tetrodotoxin-resistant (TTXr) sodium channels are selectively expressed in a specific subpopulation of nociceptive primary afferent neurons. Chronic pain caused by inflammation or nerve injury can induce changes in the function and expression of TTXr. Selective " knock down " the expression of TTXr protein with specific antisense oligodeoxynueleotide prevents hyperalgesia and allodynia. These results suggest that TTXr sodium channels may play an important role in nociception and serve as the pharmacological targets in pain control.更多还原