Morphological changes in rat brain with different types of diffuse axonal injuries
10.3760/cma.j.issn.1671-8925.2010.01.005
- VernacularTitle:大鼠脑弥漫性轴索损伤不同轴索损伤类型的形态学观察
- Author:
Hong-Cai WANG
1
;
Fang-Fang WU
;
Zhi-Xin DUAN
;
Hong ZHANG
;
Zhi-An ZHU
;
Yan-Bin MA
Author Information
1. 上海交通大学医学院附属第三人民医院
- Keywords:
Diffuse axonal injury;
β-Amyloid precursor protein;
Neurofilament;
Injury mechanism
- From:
Chinese Journal of Neuromedicine
2010;9(1):20-23
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the morphological changes of different types of axonal injury in acute stage in rat brain with diffuse axonal injury(DAD caused by combined head injuries,and explore their relevant injury mechanisms. Methods SD rats were randomized into experimental (n=16)and normal control(=8)groups.According to the different injury times(6,24 h),the experimental group was equally divided into two subgroups(n=8).A new experimental facility was employed to induce DAI in rats.HE staining was conducted in different time points in the acute stage.Immunofluorescence assay was performed to detect the expressions of antibodies to β-Amyloid precursor protein(β-APP)and antibodies to neurofilament-68(NF-68)and electron microscope was also introduced to investigate the changes of axonemal ultrastructure.Results All injured rats experienced behavioral suppression:the coma in the experimental group was significantly prolonged as compared to that in the normal control group(P<0.05).Immunofluorescence assay for antibodies to β-APP and NF-68 revealed two distinct types of axonal injuly: β-APP confined to focal spheroidal axonal swellings and axonal retraction bulbs;while NF-68 Was only found within thin and elongate axonal segments. Electron microscope also demonstrated two different types of ultrastructure of axonal injury. Conclusion Impaired axonal transport and neurofilament compaction can occur independently in the process of axonal injury with different morphological changes.Multiple immunocytochemical approaches can help to fully assess the overall axonai response to traumatic brain injury.
