ERK is Involved in Tooth-pressure-induced Fos Expression in Vc Neurons
ERK is Involved in Tooth-pressure-induced Fos Expression in Vc Neurons
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DOI：
10.1177/0022034512462397
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发表时间：
2012-12-01
影响因子：
7.6
通讯作者：
Iwata, K.
中科院分区：
文献类型：
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作者：
Hasegawa, M.;Kondo, M.;Iwata, K.
正畸治疗中遇到的不适和疼痛是患者面临的主要问题，但其潜在的神经过程和分子机制的细节尚不清楚。在本研究中，我们发现正畸弹力所产生的有害牙齿机械压力导致三叉神经脊束内亚核和尾侧移行区(Vi/Vc)、三叉神经脊束核尾侧亚核(Vc)和上颈髓(Vc/C2)细胞外信号调节蛋白激酶(ERK)的快速和瞬时激活。磷酸化ERK(PERK)仅见于神经元，而在星形胶质细胞和小胶质细胞中未见。单平面扫描分析表明，PERK定位于Vc神经元的胞核。此外，牙齿机械压力导致PERK阳性VC神经元中Fos的表达，这种表达可被鞘内注射MEK1/2抑制剂(PD98059)所抑制。综上所述，这些发现表明，牙齿受到有害的机械压力后，ERK信号通路的激活调节了VC神经元中Fos的表达，从而可能参与了与正畸治疗相关的疼痛。
Discomfort and pain encountered during orthodontic treatment are major problems for patients, but the details of the underlying neural processes and molecular mechanisms are not well-understood. Here we show that noxious tooth mechanical pressure induced by orthodontic elastics resulted in a rapid and transient activation of extracellular signal-regulated protein kinase (ERK) in the trigeminal spinal subnucleus interpolaris and caudalis transition zone (Vi/Vc), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (Vc/C2). The phosphorylated ERK (pERK) was observed in neurons but not in astroglia and microglia. Single-plane scanning analysis indicated that the pERK was localized to the nucleus of Vc neurons. In addition, the tooth mechanical pressure led to Fos expression in the pERK-positive Vc neurons that would be suppressed by intrathecal administration of an MEK1/2 inhibitor (PD98059). Taken together, these findings suggest that activation of the ERK signaling cascade following noxious mechanical pressure on the teeth regulates Fos expression in Vc neurons and may thereby contribute to pain associated with orthodontic treatment.