Increased expression of neurotrophins and their receptors in the mechanically compressed spinal cord of the spinal hyperostotic mouse (twy/twy)

Increased expression of neurotrophins and their receptors in the mechanically compressed spinal cord of the spinal hyperostotic mouse (twy/twy)
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DOI:
10.1007/s00401-003-0691-4
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发表时间:
2003-07-01
影响因子:
12.7
通讯作者:
Nakajima, H
Nakajima, H
中科院分区:
医学1区
文献类型:
--
作者:
Uchida, K;Baba, H;Nakajima, H

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本研究的目的是确定在慢性压迫的脊髓和相邻节段的网站的任何代偿性变化。为此,对24只12-24周龄的Yoshimura小鼠(twy/twy)进行了内源性脑源性神经营养因子(BDNF)、神经营养因子(NT)-3及其受体trkB和trkC的表达水平的系列免疫组织化学和免疫印迹分析。twy小鼠在C1-C2节段后部表现出自发性钙化沉积,压迫脊髓。BDNF,NT-3,trkB和trkC的免疫反应优先定位于灰质,特别是在前角细胞。在24周龄的twy小鼠严重压缩,这些神经营养因子的表达水平在网站的最大压缩显着低于在较少或非压缩网站。而BDNF、NT-3、trkB和trkC的表达水平在吻侧显著升高。和紧邻最大压迫部位的尾部部位。在12周龄的twy小鼠或癌症研究所的对照小鼠中没有发现这种变化。我们的研究结果表明,BDNF,NT-3,trkB和trkC的过度表达的运动神经元区域附近的网站的机械压缩可能代表代偿性的变化,在受损的神经元功能的压缩水平,这些蛋白质可能有助于神经元的生存和可塑性。
The purpose of the present study was to identify any compensatory changes at the site of chronic compression of the spinal cord and neighboring segments. For this purpose, serial immunohistochemical and immunoblot analyses were performed for the expression levels of endogenous brain-derived neurotrophic factor (BDNF), neurotrophin (NT)-3, and their receptors, trkB and trkC in 24 tip-toe walking Yoshimura mice (twy/twy) aged 12-24 weeks. The twy mouse exhibits spontaneous calcified deposits posteriorly at the C1-C2 level, compressing the spinal cord. Immunoreactivities for BDNF, NT-3, trkB and trkC were preferentially localized in the gray matter, particularly in the anterior horn cells. In 24-week-old twy mice with severe compression, expression levels of these neurotrophins at the site of maximal compression were significantly lower than at the less- or non-compressed sites. In contrast, the expression levels of BDNF, NT-3, trkB and trkC were significantly higher at the rostral. and caudal sites immediately adjacent to the maximal compression site. No such changes were noted in 12-week-old twy mice or in control Institute of Cancer Research mice. Our results suggest that overexpression of BDNF, NT-3, trkB and trkC in motoneuron areas neighboring the site of mechanical compression may represent compensatory changes in response to the compromised neuronal function at the level of compression, and that these proteins possibly contribute to neuronal survival and plasticity.