Effects of exogenous galanin on neuropathic pain state and change of galanin and its receptors in DRG and SDH after sciatic nerve-pinch injury in rat.
Effects of exogenous galanin on neuropathic pain state and change of galanin and its receptors in DRG and SDH after sciatic nerve-pinch injury in rat.
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DOI：
10.1371/journal.pone.0037621
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Li Z
中科院分区：
文献类型：
--
作者：
Xu X;Yang X;Zhang P;Chen X;Liu H;Li Z
大量的神经解剖学、神经生理学和神经化学机制被认为有助于神经病理性疼痛的发展和维持。然而，神经性疼痛的机制尚未完全阐明。已经证明神经肽甘丙肽（Gal）在背根神经节（DRG）和脊髓背角（SDH）损伤后上调，其中其主要起抗伤害感受作用。本研究采用大鼠坐骨神经夹伤模型，观察外源性半乳糖（Gal）对大鼠背根神经节（DRG）和琥珀酸脱氢酶（SDH）Gal及其受体（GalR 1、GalR 2）表达、痛行为、神经传导速度（NCV）和坐骨神经形态学的影响。结果表明，外源性半乳糖对神经夹伤引起的神经病理性疼痛动物模型具有抗伤害性作用。神经损伤和鞘内注射外源性Gal后，Gal、GalR 1和GalR 2在DRG和SDH中的表达发生明显变化。形态学观察显示神经夹伤后损伤严重，外源半乳糖处理后修复性再生。这些发现意味着Gal通过激活GalR 1和/或GalR 2可能在减少神经病理性疼痛行为和改善神经损伤后的神经再生方面具有神经保护作用。
A large number of neuroanatomical, neurophysiologic, and neurochemical mechanisms are thought to contribute to the development and maintenance of neuropathic pain. However, mechanisms responsible for neuropathic pain have not been completely delineated. It has been demonstrated that neuropeptide galanin (Gal) is upregulated after injury in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) where it plays a predominantly antinociceptive role. In the present study, sciatic nerve-pinch injury rat model was used to determine the effects of exogenous Gal on the expression of the Gal and its receptors (GalR1, GalR2) in DRG and SDH, the alterations of pain behavior, nerve conduction velocity (NCV) and morphology of sciatic nerve. The results showed that exogenous Gal had antinociceptive effects in this nerve-pinch injury induced neuropathic pain animal model. It is very interesting that Gal, GalR1 and GalR2 change their expression greatly in DRG and SDH after nerve injury and intrathecal injection of exougenous Gal. Morphological investigation displays a serious damage after nerve-pinch injury and an amendatory regeneration after exogenous Gal treatment. These findings imply that Gal, via activation of GalR1 and/or GalR2, may have neuroprotective effects in reducing neuropathic pain behaviors and improving nerve regeneration after nerve injury.
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影响因子：
3.3
作者：
Hulse RP;Wynick D;Donaldson LF
通讯作者：
Donaldson LF
影响因子：
2.8
作者：
Coronel, Maria Florencia;Brumovsky, Pablo Rodolfo;Villar, Marcelo Jose
通讯作者：
Villar, Marcelo Jose
影响因子：
2.9
作者：
Jin, Wu-Yang;Liu, Zhuo;Yu, Long-Chuan
通讯作者：
Yu, Long-Chuan
影响因子：
5.3
作者：
Djouhri, L;Koutsikou, S;Lawson, SN
通讯作者：
Lawson, SN
影响因子：
7.4
作者：
Flatters, SJL;Fox, AJ;Dickenson, AH
通讯作者：
Dickenson, AH