Contribution of TRPV1 receptor-expressing fibers to spinal ventral root after-discharges and mechanical hyperalgesia in a spared nerve injury (SNI) rat model.
Contribution of TRPV1 receptor-expressing fibers to spinal ventral root after-discharges and mechanical hyperalgesia in a spared nerve injury (SNI) rat model.
复制标题
TRPV1 受体表达纤维对幸存神经损伤 (SNI) 大鼠模型中脊髓腹侧根后放电和机械痛觉过敏的贡献。
DOI：
10.1254/jphs.12213fp
复制
发表时间：
2013
影响因子：
3.5
通讯作者：
H. Ono
中科院分区：
文献类型：
--
作者：
Shohei Yamamoto;M. Ohsawa;H. Ono
神经性疼痛引起异常性疼痛和痛觉过敏。在SNI模型中，明显的机械性痛觉过敏表现为针刺激后足爪退出持续时间延长。我们之前曾报道过，在麻醉的脊髓化大鼠中，在相应的后爪停止有害机械刺激后，脊髓腹侧根放电（后放电）延长。由于这些放电后通过瞬时受体电位（TRP） v1阳性纤维发生，这些纤维可能导致机械性痛觉过敏。因此，我们研究了强力TRPV1激动剂树脂干扰素选择性删除TRPV1阳性纤维是否会影响SNI大鼠的行为改变和腹侧根放电。SNI诱导的Wistar大鼠出现von Frey试验中的机械异常性痛、针刺激后的机械痛觉过敏和腹侧根放电增强，但足底试验中未出现热痛觉过敏。用树脂干扰素治疗可消除机械性痛觉过敏，而机械性异常性痛觉不受影响。此外，树脂干扰素完全消除后排放。这些结果表明，trpv1阳性纤维不参与a β-纤维致敏引起的机械性异常痛，但参与SNI后放电后和机械性痛觉过敏的增强。这表明产生机械异常性痛的机制不同于延长机械痛觉过敏的机制。
Neuropathic pain induces allodynia and hyperalgesia. In the spared nerve injury (SNI) model, marked mechanical hyperalgesia is manifested as prolongation of the duration of paw withdrawal after pin stimulation. We have previously reported that spinal ventral root discharges (after-discharges) after cessation of noxious mechanical stimulation applied to the corresponding hindpaw were prolonged in anesthetized spinalized rats. Since these after-discharges occurred through transient receptor potential (TRP) V1-positive fibers, these fibers could contribute to mechanical hyperalgesia. Therefore, we examined whether selective deletion of TRPV1-positive fibers by resiniferatoxin, an ultrapotent TRPV1 agonist, would affect the behavioral changes and ventral root discharges in SNI rats. Mechanical allodynia in the von Frey test, mechanical hyperalgesia after pin stimulation, and enhancement of ventral root discharges, but not thermal hyperalgesia in the plantar test, appeared in Wistar rats with SNI. Mechanical hyperalgesia was abolished by treatment with resiniferatoxin, whereas mechanical allodynia was not affected. Moreover, resiniferatoxin eliminated after-discharges completely. These results show that TRPV1-positive fibers do not participate in the mechanical allodynia caused by sensitization of Aβ-fibers, but contribute to the enhancement of after-discharges and mechanical hyperalgesia following SNI. It is suggested that the mechanisms responsible for generating mechanical allodynia differ from those for prolongation of mechanical hyperalgesia.
DOI：
10.1016/j.jpain.2009.09.008
发表时间：
2010-04
期刊：
The journal of pain
影响因子：
--
作者：
Corder G;Siegel A;Intondi AB;Zhang X;Zadina JE;Taylor BK
通讯作者：
Taylor BK