The anti-allodynic α2δ ligand pregabalin inhibits the trafficking of the calcium channel α2δ-1 subunit to presynaptic terminals in vivo

被引:75
作者
Bauer, Claudia S.
Rahman, Wahida
Tran-Van-Minh, Alexandra
Lujan, Rafael [1 ]
Dickenson, Anthony H.
Dolphin, Annette C.
机构
[1] Univ Castilla La Mancha, Dept Ciencias Med, Albacete 02006, Spain
基金
英国生物技术与生命科学研究理事会; 英国惠康基金;
关键词
alpha(2)delta-1; neuropathic pain; pregabalin; spinal nerve ligation; trafficking; voltage-gated calcium channel; DORSAL-ROOT GANGLION; NEUROPATHIC PAIN; UP-REGULATION; MECHANISMS; CONTRIBUTES; GABAPENTIN; EXPRESSION; HORN;
D O I
10.1042/BST0380525
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Neuropathic pain is caused by lesion or dysfunction of the peripheral sensory nervous system Up-regulation of the voltage-gated Ca2+ channel subunit alpha(2)delta-1 in DRG (dorsal root ganglion) neurons and the spinal cord correlates with the onset of neuropathic pain symptoms such as allodynia in several animal models of neuropathic pain. The clinically important anti-allodynic drugs gabapentin and pregabalin are alpha(2)delta-1 ligands, but how these drugs alleviate neuropathic pain is poorly understood. In the present paper, we review recent advances in our understanding of their molecular mechanisms.
引用
收藏
页码:525 / 528
页数:4
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