Nelson Michael T, Todorovic Slobodan M
Department of Anesthesiology, University of Virginia Health System, Charlottesville, VA, USA.
Mol Neurobiol. 2006 Dec;34(3):243-8. doi: 10.1385/MN:34:3:243.
Following tissue injury, both peripheral and central sensory neurons can become hyperexcitable, or "sensitized." Sensitization can lead to long-term pathological changes in pain sensation. Because many chronic pain conditions are refractory to most currently available treatments, there is great interest in identifying molecular targets that contribute to the sensitization of sensory neurons. Among these, several classes of ion channels have emerged as potential targets. Recent in vitro and in vivo studies have demonstrated a role for T-type Ca2+ channels in sensory pathways and have suggested that these channels may contribute to pain processing and sensitization. Therefore, T-type channels may represent an opportunity for the development of novel pain therapeutics and may help to address an unmet medical need.
组织损伤后,外周和中枢感觉神经元均可变得过度兴奋,即“敏化”。敏化可导致痛觉的长期病理变化。由于许多慢性疼痛病症对目前大多数可用治疗方法均具有抗性,因此人们对确定导致感觉神经元敏化的分子靶点极为关注。其中,几类离子通道已成为潜在靶点。最近的体外和体内研究已证明T型Ca2+通道在感觉通路中发挥作用,并表明这些通道可能参与疼痛处理和敏化过程。因此,T型通道可能为新型疼痛治疗药物的开发提供契机,并可能有助于满足尚未得到满足的医疗需求。