Gene transfer of glutamic acid decarboxylase reduces neuropathic pain
Gene transfer of glutamic acid decarboxylase reduces neuropathic pain
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DOI：
10.1002/ana.20483
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发表时间：
2005-06-01
影响因子：
11.2
通讯作者：
Fink, DJ
中科院分区：
文献类型：
--
作者：
Hao, SG;Mata, M;Fink, DJ
我们测试了是否转移编码谷氨酸脱羧酶的基因到背根神经节使用单纯疱疹病毒载体，以实现释放GABA在背角将减弱在这种情况下的伤害性感受。皮下接种的复制缺陷型单纯疱疹病毒载体表达谷氨酸脱羧酶（载体QHGAD 67）7天后，选择性L5脊神经结扎逆转机械异常性疼痛和热痛觉过敏，抗异常性疼痛的效果持续6周，并重新建立了接种。QHGAD 67接种还抑制脊髓中c-Fos和磷酸化细胞外信号调节激酶I和2的诱导。
We tested whether transfer of the gene coding for glutamic acid decarboxylase to dorsal root ganglion using a herpes simplex virus vector to achieve release of GABA in dorsal horn would attenuate nociception in this condition. Subcutaneous inoculation of a replication-defective herpes simplex virus vector expressing glutamic acid decarboxylase (vector QHGAD67) 7 days after selective L5 spinal nerve ligation reversed mechanical allodynia and thermal hyperalgesia; the antiallodynic effect lasted 6 weeks and was reestablished by reinoculation. QHGAD67 inoculation also suppressed induction of c-Fos and phosphorylated extracellular signal-regulated kinase I and 2 in the spinal cord.