Cellular reactions to axotomy in rat superior cervical ganglia includes apoptotic cell death
Cellular reactions to axotomy in rat superior cervical ganglia includes apoptotic cell death
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DOI：
10.1023/a:1006988528655
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发表时间：
1998-06-01
期刊：
影响因子：
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通讯作者：
Dahlström, AB
中科院分区：
文献类型：
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作者：
Hou, XE;Lundmark, K;Dahlström, AB
横断颈内和颈外神经后，每隔 6 小时至 14 天，通过免疫荧光检查颈上神经节对轴突损伤的细胞反应。轴突切除术后 1 天，神经节中的一些神经元出现 GAP-43 免疫反应性 (IR)，而对照神经节中的神经元呈 GAP-43 阴性。 3天后，轴突切断的神经节GAP-43-IR结构在神经纤维束的数量和强度上增加，而GAP-43阳性的核周体仅限于神经节的中部和尾部，并且显示出比轴突切断后1天更强的强度。这些 GAP-43 阳性神经元也是甘丙肽阳性。在神经节的颅部，轴突切除后 18 小时，卫星细胞中的 S100-IR 较弱。在该区域的外围，S100-IR 更强，并且与 HSP-72-IR 共定位，优先位于卫星小区中。然而，在轴突切除后 1 天和 3 天的主要神经元中偶尔也观察到 HSP-72-IR。在伊红染色切片中，1天轴突神经节颅部的神经元和卫星细胞数量减少，并且在3天时注意到进一步损失。 12小时时，神经节颅部的一些卫星细胞被原位DNA 3'端标记方法标记，表明细胞凋亡，并且在1g小时时许多细胞被标记。一些神经元周核也在该区域被标记。在轴突切除后 1 天或之后未观察到标记，在对照神经节中也未观察到标记。结果可能意味着，不仅神经元而且卫星细胞也会通过细胞凋亡对神经元轴突损伤做出反应。神经节中部和尾部的神经元存活下来，并显示 GAP-43 和甘丙肽含量增加，这可能是再生/神经元可塑性的标志。
The cellular response to axonal injury in the superior cervical ganglion was examined by immunofluoresence at intervals from 6 h to 14 days after transection of the internal and external carotid nerves. GAP-43-immunoreactivity (IR) appeared in some neurons in the ganglia 1 day after axotomy, while neurons in control ganglia were GAP-43 negative. In 3 days axotomized ganglia GAP-43-IR structures were increased in number and intensity in nerve fiber bundles, while GAP-43-positive perikarya were restricted to the middle and caudal parts of the ganglia and showed an intensity that was stronger than at 1 day after axotomy. These GAP-43-positive neurons were also galanin positive. In the cranial part of the ganglia, S100-IR in satellite cells was weak at 18 h after axotomy. Peripheral to this area, S100-IR was stronger and co-localized with HSP-72-IR, preferentially located in satellite cells. HSP-72-IR was, however, occasionally observed also in principal neurons at 1 and 3 days after axotomy. In eosin-stained sections, neurons and satellite cells in the cranial part of 1 day axotomized ganglia were reduced in number, and a further loss was noted at 3 days. At 12 h some satellite cells in the cranial part of the ganglia were labelled by the in situ DNA 3'-end labelling method, indicating apoptosis, and at Ig h many cells were labelled. Some neuronal perikarya were also labelled in this region. Labelling was not observed at 1 day or later after axotomy, nor in control ganglia. The results may imply that not only neurons but also satellite cells react to neuronal axonal injury with apoptosis. Neurons in the middle and caudal part of the ganglia survived and showed increased content of GAP-43 and galanin, possibly a sign of regeneration/neuronal plasticity.