Influence of mitochondrial deficiency on expression of microtubule-associated proteins in primary cultured hippocampal neurons of neonatal rats
- VernacularTitle:线粒体缺陷对原代培养新生大鼠海马神经元微管相关蛋白表达的影响
- Author:
Lan ZHANG
;
Wenlin AN
;
Lin LI
;
Bing XUE
;
Liqin BAN
;
Xiaoming LI
;
Yanling XU
;
Shuse LIU
- Publication Type:Journal Article
- Keywords:
Microtubule-associated proteins;
Hippocampus;
Neurons;
Mitochondria;
Alzheimer's disease
- From:
Chinese Journal of Pathophysiology
2000;0(12):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: In order to study the relationship between mitochondrial deficiency and Alzheimer's disease(AD), we used sodium azide, a specific inhibitor of cytochrome C oxidase(COX), to develop a cell model of mitochondrial complex IV deficiency and investigated the impairment of microtubules and microtubule-associated proteins. METHODS: Primary cultured hippocampal neurons of hewborn rats were exposed to sodium azide ,then cell viability was measured by MTT method; cell morphology, immunofluorecence-stained cellular microtubules and microtubule-associated proteins were observed by confocal microscopy. RESULTS: Primary cultured hippocampal neurons were exposed to 8-128 mmol/L sodium azide for 3-24 h, MTT absorbance decreased dose-and time-dependently. Exposed to 64 mmol/L sodium azide for 6 h, the processes of cells retracted, synapses disappeared, axons were shortened under contrast microscope. Meanwhile, microtubles were disassembled and became disorderly, the expression of microtubule-associated proteins were also reduced especially in the processes observed by confocal microscopy. CONCLUSIONS: Sodium azide inhibits the assembly and polymerization of tubulin in microtubules which may be reduced by low expression of microtubule-associated proteins in nerve cells. The damage of axons induced by microtubule collapse further blocks the intercellular signal transduction and intracellular material transportation which are important causes in cell death.
