Abstract

The aim of study was to investigate characteristics of neurodystrophic changes in neurons and glia of the motor cortex in rats with different levels of cognitive functions under bilateral ligation of the common carotid arteries. Material and methods . The study included 136 Wistar rats. All animals were divided into two subgroups based on the results of the Morris water maze test: with high and low level of ability to spatial learning. Animals of the experimental group were removed from the experiment on the 1st, 6th, 14th, 21st, 35th, 60th and 90th days after bilateral ligation of both carotid arteries. Histological sections of the motor cortex were studied using Nissl and hematoxylin-eosin staining. Results . In 1, 6 and 8 days after ischemia, the number of neurons with irreversible changes and dead cells reached their maximum for the entire time of observation. On the 8th day of study, compact groups of glial cells appeared near the vessels. Heterochrony was noted: in animals with high level of cognitive ability, an increase in the number of neurons with irreversible changes followed the peak of cell death; in animals with low level, on the contrary, the maximum number of dead cells was observed on the 6th day, and the maximum number of neurons with irreversible changes – on the 1st. On the 14th, 21st, and 28th days there was observed a gradual stabilization of indicators characterizing damage to the cerebral cortex. Average values of the perikarya area and neurons nuclei increased, the nuclear-cytoplasmic ratio decreased, and intracellular swelling was noted. After 35 days, areas of the cortex depleted in bodies of neurons and glia appeared; the number of neurons with irreversible changes increased, to a greater extent, in animals with high level of cognitive abilities. Typical trends of the first month of study are as follows: a decrease in the nuclear-cytoplasmic ratio and a number of neurons without irreversible changes, and an increase in the neuroglial index continued to progress on the 60th and 90th days of study. The apical dendrites of the pyramidal neurons obtained a corkscrew course. Compact groups of glial cells disappeared. Conclusion . During the first week of cerebral hypoperfusion, irreversible changes in neurons predominated, in the second and third weeks, the morphological criteria of their functional activity decreased. In the fourth and fifth weeks incomplete adaptation developed in the form of an increased number of neurons near the vessels of the hemocirculatory bed and an increased number of satellite gliocytes by immersing them in the cytoplasm of neurons. In 2-3 months after cerebral hypoperfusion, signs of acute hypoxia reappeared. Animals with high level of cognitive ability were characterized by large damage to the structures of the neuroglial ensemble.

Highlights

  • Изменения клеточного состава коры головного мозга у крыс с разным уровнем когнитивных функций при церебральной гипоперфузии

  • In 1, 6 and 8 days after ischemia, the number of neurons with irreversible changes and dead cells reached their maximum for the entire time of observation

  • Heterochrony was noted: in animals with high level of cognitive ability, an increase in the number of neurons with irreversible changes followed the peak of cell death; in animals with low level, on the contrary, the maximum number of dead cells was observed on the 6th day, and the maximum number of neurons with irreversible changes – on the 1st

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Summary

Material and methods

All animals were divided into two subgroups based on the results of the Morris water maze test: with high and low level of ability to spatial learning. Animals of the experimental group were removed from the experiment on the 1st, 6th, 14th, 21st, 35th, 60th and 90th days after bilateral ligation of both carotid arteries. Histological sections of the motor cortex were studied using Nissl and hematoxylin-eosin staining

Results
Conclusion
Материал и методы исследования
Результаты и их обсуждение
Площадь ядра
Количество глии рядом с ГК
Smolenskoy Gosudarstvennoy Meditsinskoy
Vascular Complexes of the Brain After Acute
Full Text
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