Model of The Global Cerebral Ishemia in Mongolian Gerbil

DOI: 10.29296/2618723X-2019-02-03

V.Vavilova, Ya. Gushin

Research-and-manufacturing company «Home оf Pharmacy»
188663, Russia, Leningradskiy region, Vsevolozhskiy district, Kuzmolovskiy, Zavodskaya st., b. 245, 3
E-mail: [email protected]

Keywords: mongolian gerbil global cerebral ischemia stroke

For citation:

Vavilova V., Gushin Ya. Model of The Global Cerebral Ishemia in Mongolian Gerbil. Laboratory Animals for Science. 2019; 2.


The aim of this study was to develop a global cerebral ischemia simulation protocol (GCI, global cerebral ischemia) with subsequent reperfusion, which was carried out on Mongolian gerbil. The choice of a gerbil as a biological model is due to the anatomical feature of the blood supply to the brain. Gerbils, unlike other laboratory animals and humans, do not have a posterior communicating artery (do not have the full circle of Willis). Mortality, neurological status, pathological and histological studies were evaluated as criteria for the pathology degree estimation. Visualization of the ischemic region after the induction of pathology was carried out by staining brain sections with 2,3,5 triphenyl tetrazolium chloride (TTC). The method of the neurological status scoring which takes into account the presence or absence of pathological changes is described. The model is confirmed by pathological and histological examination. The severity of damage prevails on the 2nd and to a lesser extent on the 3rd day after the pathology induction. Histological examination of the gerbil brain identified neurons with signs of dystrophy (polymorphic, hyperchromic cells with fuzzy contours - “red” neurons) and reduced in size - “shadow cells”, as well as fields with mild gliosis in the cerebral cortex and cerebellar cortex. Thus, the results of the study showed that the 20-minute bilateral occlusion resulted in animal survival of about 60%, most animals demonstrated pronounced neurological deficit. Staining with TTC has shown that it is advisable to evaluate volume of the ischemic lesion in the first 24 hours after the induction of pathology. In addition, results showed that the neurological deficit was most pronounced during first 4 days after occlusion. To estimate long-lasting pathological changes it is advisable to conduct a histological examination of brain tissue samples.

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