Involvement of GluR2 and GluR3 subunit C-termini in the trigeminal spinal subnucleus caudalis and C1-C2 neurons in trigeminal neuropathic pain.
Involvement of GluR2 and GluR3 subunit C-termini in the trigeminal spinal subnucleus caudalis and C1-C2 neurons in trigeminal neuropathic pain.
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DOI：
10.1016/j.neulet.2010.12.060
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发表时间：
2011-03-10
影响因子：
2.5
通讯作者：
Iwata K
中科院分区：
文献类型：
--
作者：
Miyamoto M;Tsuboi Y;Takamiya K;Huganir RL;Kondo M;Shinoda M;Oi Y;Iwata K
为了阐明AMPA受体的GluR 2和GluR 3亚基在口面神经病理性疼痛中的参与，我们研究了GluR 2或GluR 3 delta 7敲入（KI）小鼠在眶下神经（ION）部分横断模型后疼痛反应行为和细胞外信号调节激酶（ERK）磷酸化的变化。在这些动物中，GluR 2或GluR 3亚基的最后7个氨基酸，相互作用蛋白的结合位点，在体内被删除。头回阈值机械刺激的同侧的胡须垫皮肤离子部分横断后1，3，5，7，11和14天的野生型小鼠与横断前相比，显着降低。在GluR 2和GluR 3 delta 7 KI小鼠中，头退缩阈值在离子部分横断后没有变化。非伤害性刺激后，野生型小鼠Vc和C1-C2中检测到的pERK-LI细胞数量大于GluR 2和GluR 3 delta 7 KI小鼠。提示AMPA受体GluR 2和GluR 3亚单位在三叉神经损伤后Vc和C1-C2神经元兴奋性增强和痛觉过敏中起作用。
To clarify the involvement of GluR2 and GluR3 subunits of AMPA receptor in orofacial neuropathic pain, we studied changes in nocifensive behavior and extracellular-signal regulated kinase (ERK) phosphorylation followed by infraorbital nerve (ION)-partial transection model applied to GluR2 or GluR3 delta7 knock-in (KI) mice. In these animals, last seven amino acids of GluR2 or GluR3 subunit, the binding sites of interacting protein, are deleted in vivo. Head-withdrawal threshold to mechanical stimulation of the whisker pad skin ipsilateral to ION-partial transection was significantly reduced at 1, 3, 5, 7, 11 and 14 days after transection compared with that before transection in wild-type mice. In the GluR2 and GluR3 delta7 KI mice, the head-withdrawal threshold did not change following ION-partial transection. The number of pERK-LI cells examined in Vc and C1–C2 in wild-type mice after the non-noxious stimulation was larger than that of GluR2 and GluR3 delta7 KI mice. The present findings suggest that GluR2 and GluR3 subunits of AMPA receptor play roles in the trigeminal nerve injury-mediated enhancement of Vc and C1–C2 neuronal excitability, and hyperalgesia.
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