Brain-derived neurotrophic factor enhances the excitability of small-diameter trigeminal ganglion neurons projecting to the trigeminal nucleus interpolaris/caudalis transition zone following masseter muscle inflammation.
Brain-derived neurotrophic factor enhances the excitability of small-diameter trigeminal ganglion neurons projecting to the trigeminal nucleus interpolaris/caudalis transition zone following masseter muscle inflammation.
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DOI：
10.1186/1744-8069-9-49
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发表时间：
2013-09-30
期刊：
影响因子：
3.3
通讯作者：
Matsumoto S
中科院分区：
文献类型：
--
作者：
Takeda M;Takahashi M;Kitagawa J;Kanazawa T;Nasu M;Matsumoto S
三叉神经内插/尾侧过渡区（Vi/Vc）在口面部深度疼痛中起重要作用，但主要传入投射到Vi/Vc的作用尚不清楚。本研究探讨痛觉过敏对咬肌（MM）炎症后三叉神经节（TRG）神经元脑源性神经营养因子(BDNF)-酪氨酸激酶B （trkB）信号系统的功能意义。炎症MM以上皮肤机械刺激的逃逸阈值明显低于naïve大鼠。用荧光金（FG）标记支配MM的TRG神经元，用微珠（MB）标记投射到Vi/Vc区的神经元。FG/ mb标记的TRG神经元对BDNF和trkB有免疫反应（IR）。炎症大鼠BDNF/trkB-IR小/中径TRG神经元的平均数量明显高于naïve大鼠。在全细胞电流钳实验中，大多数解离的小直径TRG神经元对BDNF表现出去极化反应，并与尖峰放电相关，炎症大鼠中引起去极化反应的BDNF浓度显著降低。此外，在炎症大鼠中，注射电流时bdnf诱导的峰值的相对数量显著增加。酪氨酸激酶抑制剂K252a可消除bdnf诱导的TRG神经元兴奋性变化。本研究提供了BDNF增强MM炎症后小直径TRG神经元投射到Vi/Vc的兴奋性的证据。这些发现提示神经节BDNF-trkB信号是治疗三叉神经节炎性痛觉过敏的一个治疗靶点。
The trigeminal subnuclei interpolaris/caudalis transition zones (Vi/Vc) play an important role in orofacial deep pain, however, the role of primary afferent projections to the Vi/Vc remains to be determined. This study investigated the functional significance of hyperalgesia to the brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (trkB) signaling system in trigeminal ganglion (TRG) neurons projecting to the Vi/Vc transition zone following masseter muscle (MM) inflammation. The escape threshold from mechanical stimulation applied to skin above the inflamed MM was significantly lower than in naïve rats. Fluorogold (FG) labeling was used to identify the TRG neurons innervating the MM, while microbeads (MB) were used to label neurons projecting to the Vi/Vc region. FG/MB-labeled TRG neurons were immunoreactive (IR) for BDNF and trkB. The mean number of BDNF/trkB-IR small/medium-diameter TRG neurons was significantly higher in inflamed rats than in naïve rats. In whole-cell current-clamp experiments, the majority of dissociated small-diameter TRG neurons showed a depolarization response to BDNF that was associated with spike discharge, and the concentration of BDNF that evoked a depolarizing response was significantly lower in the inflamed rats. In addition, the relative number of BDNF-induced spikes during current injection was significantly higher in inflamed rats. The BDNF-induced changes in TRG neuron excitability was abolished by tyrosine kinase inhibitor, K252a. The present study provided evidence that BDNF enhances the excitability of the small-diameter TRG neurons projecting onto the Vi/Vc following MM inflammation. These findings suggest that ganglionic BDNF-trkB signaling is a therapeutic target for the treatment of trigeminal inflammatory hyperalgesia.
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影响因子：
3.3
作者：
Balkowiec-Iskra, E.;Vermehren-Schmaedick, A.;Balkowiec, A.
通讯作者：
Balkowiec, A.
影响因子：
5.3
作者：
Guo, W;Robbins, MT;Ren, K
通讯作者：
Ren, K
影响因子：
5.3
作者：
Balkowiec, A;Katz, DM
通讯作者：
Katz, DM
影响因子：
2.9
作者：
Cho, HJ;Kim, SY;Chu, MY
通讯作者：
Chu, MY
影响因子：
2.3
作者：
Drake-Baumann, R
通讯作者：
Drake-Baumann, R