Expression of brain-derived neurotrophic factor and its receptors in the median eminence cells with sensitivity to stress
Expression of brain-derived neurotrophic factor and its receptors in the median eminence cells with sensitivity to stress
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DOI：
10.1210/en.2004-0616
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发表时间：
2004-10-01
期刊：
影响因子：
4.8
通讯作者：
Tapia-Arancibia, L
中科院分区：
文献类型：
--
作者：
Givalois, L;Arancibia, S;Tapia-Arancibia, L
正中隆起（ME）被认为是连接神经系统和内分泌系统的最后共同通路。在这种神经血管结构中，神经末梢、伸长细胞和星形胶质细胞之间的动态相互作用通过塑性过程决定神经激素进入门静脉血。由于脑源性神经营养因子（BDNF）参与塑料的变化，我们研究了它的存在和它的受体（TrkB）在不同的细胞类型中所描述的ME。使用原位杂交和免疫组化技术，我们证明，BDNF免疫反应性基本上是位于星形胶质细胞和在较小程度上在tanycytes。相比之下，在到达ME外层的神经末梢中未检测到BDNF。识别细胞外受体结构域的TrkB抗体标记了所有这些不同的细胞类型，表明BDNF在该水平的自分泌或旁分泌作用。更多的选择性抗体显示，TrkB.FL免疫染色被发现在伸长细胞和神经末梢，而TrkB. T1免疫染色被定位在所有类型的细胞。固定应力增加BDNF的mRNA和BDNF的免疫反应模式，并诱导双相脑源性神经营养因子释放ME，推拉灌注分析。此外，我们观察到，60分钟的压力加强BDNF免疫反应的内层，也与胶质细胞酸性蛋白的共定位。压力也加重了BDNF免疫染色在血管周围空间的元素，没有标记抗体识别成纤维细胞或内皮细胞。这些数据揭示了BDNF及其受体在ME中的新位置，推测它们参与了激素释放等动态过程。
The median eminence (ME) is considered as the final common pathway connecting the nervous and endocrine systems. In this neurohemal structure, dynamic interactions among nerve terminals, tanycytes, and astrocytes determine through plastic processes the neurohormones access to the portal blood. Because brain-derived neurotrophic factor (BDNF) is involved in plastic changes, we investigated its presence and that of its receptors (TrkB) in the different cellular types described in the ME. Using in situ hybridization and immunohistochemical techniques, we demonstrated that BDNF immunoreactivity was essentially located in the astrocytes and to a lesser extent in tanycytes. By contrast, BDNF was not detected in nerve terminals reaching the external layer of the ME. TrkB antibodies recognizing the extracellular receptor domain labeled all of these different cell types, suggesting an autocrine or paracrine action of BDNF at this level. More selective antibodies showed that TrkB.FL immunostaining was found in tanycytes and nerve endings, whereas TrkB.T1 immunostaining was localized in all cellular types. Immobilization stress increased BDNF mRNA and BDNF immunoreactivity patterns and induced biphasic BDNF release from the ME, as analyzed by push-pull perfusion. In addition, we observed that 60-min stress intensified BDNF immunoreactivity in the internal layer and also its colocalization with glial fibrillary acidic protein. Stress also accentuated BDNF immunostaining in the perivascular space in elements that were not labeled with antibodies recognizing fibroblast or endothelial cells. These data disclosed a novel location of BDNF and its receptors in the ME, which are presumably involved in dynamic processes such as hormone release.