Tengvar C
Acta Neuropathol. 1986;71(3-4):177-89. doi: 10.1007/BF00688038.
A study was made of the uptake of horseradish peroxidase (HRP) into neurons from a cryogenic cortical lesion in the mouse brain associated with vasogenic edema, following intravenous administration of the tracer. Particular emphasis was placed on the axonal spread of HRP from the primary lesion to other areas of the central nervous system. The distribution of HRP was studied by light microscopy, using highly sensitive histochemical methods, 3-144 h after the onset of the injury. Extravasated HRP was taken up into nerve cell bodies in and around the primary lesion, forming different patterns of labelling: (1) granular, (2) diffuse, and (3) a combination of granular and diffuse staining. Granularity is considered to be the result of HRP accumulation in lysosomes occurring in undamaged or slightly damaged nerve cells, whereas the diffuse, non-granular pattern presumably occurs in severely damaged neurons. Nerve cell bodies containing HRP reaction product were also found in the contralateral cortex, ipsilateral thalamus, substantia nigra, amygdala and ventral tegmental area, presumably a consequence of retrograde axonal transport of the tracer from the primary injury. HRP-containing axons were present in the corpus callosum and in the pyramidal tract of the injured hemisphere all the way down to the cervical spinal cord. Labelling of axonal terminals and preterminal axons in the ipsilateral thalamus, entopeduncular nucleus, subthalamic nucleus, substantia nigra and pons indicated anterograde transport of HRP to these regions. Thus very extensive intraneuronal spread of a macromolecular edema component takes place from a primary focal brain lesion to areas located far away from but neuroanatomically connected to this injured region. The brain thus seems to be affected by focal vasogenic edema in many more ways than are recognized at present.
在给小鼠静脉注射示踪剂后，对与血管源性水肿相关的低温脑皮质损伤部位的神经元摄取辣根过氧化物酶（HRP）进行了研究。特别强调了HRP从原发性损伤部位向中枢神经系统其他区域的轴突扩散。在损伤发生后3 - 144小时，使用高灵敏度组织化学方法，通过光学显微镜研究HRP的分布。外渗的HRP被原发性损伤部位及其周围的神经细胞体摄取，形成不同的标记模式：（1）颗粒状，（2）弥漫性，以及（3）颗粒状和弥漫性染色的组合。颗粒状被认为是HRP在未受损或轻度受损神经细胞的溶酶体中积累的结果，而弥漫性、非颗粒状模式可能发生在严重受损的神经元中。在对侧皮质、同侧丘脑、黑质、杏仁核和腹侧被盖区也发现了含有HRP反应产物的神经细胞体，这可能是示踪剂从原发性损伤部位逆行轴突运输的结果。含有HRP的轴突存在于胼胝体和受损半球的锥体束中，一直延伸到颈脊髓。同侧丘脑、内囊核、丘脑底核、黑质和脑桥中轴突终末和终末前轴突的标记表明HRP向这些区域的顺行运输。因此，大分子水肿成分在神经元内从原发性局灶性脑损伤部位向远离该损伤区域但在神经解剖学上与之相连的区域发生了非常广泛的扩散。因此，大脑似乎受到局灶性血管源性水肿的影响，其方式比目前所认识到的要多得多。
