Involvement of AMPA receptor GluR2 and GluR3 trafficking in trigeminal spinal subnucleus caudalis and C1/C2 neurons in acute-facial inflammatory pain.
Involvement of AMPA receptor GluR2 and GluR3 trafficking in trigeminal spinal subnucleus caudalis and C1/C2 neurons in acute-facial inflammatory pain.
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DOI：
10.1371/journal.pone.0044055
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Iwata K
中科院分区：
文献类型：
--
作者：
Miyamoto M;Tsuboi Y;Honda K;Kobayashi M;Takamiya K;Huganir RL;Kondo M;Shinoda M;Sessle BJ;Katagiri A;Kita D;Suzuki I;Oi Y;Iwata K
为了评估α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPAR）GluR 2和GluR 3亚基在急性炎性口面疼痛中的参与，我们分析了GluR 2 delta 7敲入（KI）、GluR 3 delta 7 KI小鼠和野生型小鼠的伤害反应行为、磷酸化细胞外信号调节激酶（pERK）和Vi/Vc、Vc和C1/C2中的Fos表达。我们还研究了Vc神经元的活动，以解决这一假设，即运输的GluR 2和GluR 3亚基在Vi/Vc，Vc和C1/C2神经元的活动与口面炎症在这些小鼠中起着重要的作用。GluR 2 delta 7 KI和GluR 3 delta 7 KI小鼠的晚期伤害反应行为显著降低。此外，在福尔马林注射后40分钟，GluR 2 delta 7 KI和GluR 3 delta 7 KI小鼠的Vi/Vc、Vc和C1/C2中的pERK免疫反应（IR）细胞数量显著减少，与野生型小鼠相比，GluR 3 delta 7 KI小鼠的pERK免疫反应（IR）细胞数量也显著减少。福尔马林注射后40分钟，GluR 2 delta 7 KI和GluR 3 delta 7 KI小鼠同侧Vi/Vc、Vc和C1/C2中Fos蛋白IR细胞的数量也显著小于野生型小鼠。伤害性神经元在功能上被鉴定为Vc中的宽动态范围神经元，其中pERK和Fos蛋白IR细胞表达突出，在福尔马林注射后，GluR 2 delta 7 KI和GluR 3 delta 7 KI小鼠中的自发活动显著低于野生型小鼠。这些结果表明，GluR 2和GluR 3的运输参与增强Vi/Vc，Vc和C1/C2伤害性神经元的兴奋性，在16-60分钟后福尔马林注射，导致口面炎性疼痛。
To evaluate the involvement of trafficking of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) GluR2 and GluR3 subunits in an acute inflammatory orofacial pain, we analyzed nocifensive behavior, phosphorylated extracellular signal-regulated kinase (pERK) and Fos expression in Vi/Vc, Vc and C1/C2 in GluR2 delta7 knock-in (KI), GluR3 delta7 KI mice and wild-type mice. We also studied Vc neuronal activity to address the hypothesis that trafficking of GluR2 and GluR3 subunits plays an important role in Vi/Vc, Vc and C1/C2 neuronal activity associated with orofacial inflammation in these mice. Late nocifensive behavior was significantly depressed in GluR2 delta7 KI and GluR3 delta7 KI mice. In addition, the number of pERK-immunoreactive (IR) cells was significantly decreased bilaterally in the Vi/Vc, Vc and C1/C2 in GluR2 delta7 KI and GluR3 delta7 KI mice compared to wild-type mice at 40 min after formalin injection, and was also significantly smaller in GluR3 delta7 KI compared to GluR2 delta7 KI mice. The number of Fos protein-IR cells in the ipsilateral Vi/Vc, Vc and C1/C2 was also significantly smaller in GluR2 delta7 KI and GluR3 delta7 KI mice compared to wild-type mice 40 min after formalin injection. Nociceptive neurons functionally identified as wide dynamic range neurons in the Vc, where pERK- and Fos protein-IR cell expression was prominent, showed significantly lower spontaneous activity in GluR2 delta7 KI and GluR3 delta7 KI mice than wild-type mice following formalin injection. These findings suggest that GluR2 and GluR3 trafficking is involved in the enhancement of Vi/Vc, Vc and C1/C2 nociceptive neuronal excitabilities at 16–60 min following formalin injection, resulting in orofacial inflammatory pain.
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