Han Hye Min, Kim Tae Heon, Bae Jin Young, Bae Yong Chul
Department of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 700-412, South Korea.
Department of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 700-412, South Korea.
Neurosci Lett. 2019 Jan 18;690:56-60. doi: 10.1016/j.neulet.2018.10.009. Epub 2018 Oct 9.
Tropomyosin receptor kinase A (trkA), a high affinity receptor for nerve growth factor (NGF), has been implicated in neuronal survival, neurite outgrowth and inflammatory pain. So far, the characterization of the primary sensory neurons that express trkA, and are thus potentially affected by NGF, has remained incomplete. The goal of this study was to investigate the trkA-expressing neurons and fibers in the rat trigeminal ganglion and its sensory root using light- and electron-microscopic immunohistochemistry and quantitative analysis. TrkA-immunopositive (+) trigeminal neurons varied from small to large. Double immunofluorescent staining showed that about 28%, 33% and 3% of the trkA(+) neurons coexpressed SP, CGRP and IB4, respectively. About 11% of the trkA(+) neurons also coexpressed parvalbumin. Electron microscopy revealed that trkA was expressed in all types of fibers: While the large majority of the trkA(+) fibers were unmyelinated (35.3%) and small myelinated (<20 μm in cross-sectional area; 45.5%), a still considerable fraction (19.2%) was large myelinated. These findings indicate that all types of trigeminal neurons (ones with unmyelinated, small myelinated or large myelinated fibers) may be regulated by NGF/trkA signaling.
原肌球蛋白受体激酶A(trkA)是神经生长因子(NGF)的高亲和力受体,与神经元存活、神经突生长和炎性疼痛有关。到目前为止,对表达trkA因而可能受NGF影响的初级感觉神经元的特征描述仍不完整。本研究的目的是利用光镜和电镜免疫组织化学及定量分析,研究大鼠三叉神经节及其感觉根中表达trkA的神经元和纤维。trkA免疫阳性(+)的三叉神经元大小不一。双重免疫荧光染色显示,分别约有28%、33%和3%的trkA(+)神经元共表达P物质(SP)、降钙素基因相关肽(CGRP)和IB4。约11%的trkA(+)神经元还共表达小白蛋白。电子显微镜显示trkA在所有类型的纤维中均有表达:绝大多数trkA(+)纤维是无髓鞘的(35.3%)和有薄髓鞘的(横截面积<20μm;45.5%),但仍有相当一部分(19.2%)是有厚髓鞘的。这些发现表明,所有类型的三叉神经元(具有无髓鞘、薄髓鞘或厚髓鞘纤维的神经元)可能都受NGF/trkA信号通路的调节。