REACTIVE CHANGES OF THE RAT BRAIN CELL ELEMENTS DUE TO CIRCULATORY HYPOXIA



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Abstract

The research is devoted to establishment of a complex of the main structural, spatial and quantitative reactive changes of cellular elements of anterior cingulate cortex and the midbrain paranigral nucleus located in different conditions of forbrain circulator hypoxia. The data obtained will help to present differences in reactivity of the brain cells in relationship with each other and with a wall of a blood capillary, and also can be used as a basis for modeling pharmacological correction of posthypoxic conditions. Histologic sections of forward medial part of the paranigral nucleus and layers of the V-VI pregenual cingular field of adult rats in 7 days after occlusion of both general carotids were examined. The sections of intact animals and sham-operated animals were studied too. In the sections, stained after Nissl, the ratio of the low-changed, hypochromic, picnomorphic and shadow neurons, quantity of astrocytes, oligodendrocytes, microgliocytes and endotheliocytes, the viable low-changed and hypochromic neurons, astrocytes and microgliocytes cell bodies area, length of astrocytes axial shoots, distance from bodies of viable neurons and astrocytes to a wall of capillaries, the gliocyte-neuronal index were determined by methods of identification of glial fibrillar acid protein and Iba1-protein. The cellular elements of the surviving brain in different conditions of circulator hypoxia were established to characterize by a range of the expressed pathological changes. Neurons were in process of picnotization, lysis and transformation into shadow cells. Cells of the nuclear zone of hypoxia trended to death or picnosis. The neurons located outside the hypoxic area and being affected by only humoral influence of the glutamate-calcium cascade, were inclined to sharp swelling. Microgliocyte reaction in the form of poorly expressed increase in their number and structural signs of activation was an early diffusion manifestation of the forbrain focal hypoxia. Endotheliocytes proliferation in terms of early ischemic influence did not connect with a cascade reactions chain and was observed only in hypoxia focus. The concentration of viable neurons and astrocytes near blood capillaries, and also the increase of number of satellite glial forms were adaptation mechanism and condition for survival of cells under various conditions of ischemic influence on the brain.

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About the authors

A V Droblenkov

Institute of Experimental Medicine NWB RAMS

Email: pdshabanov@mail.ru

N V Naumov

Institute of Experimental Medicine NWB RAMS

M V Monid

Institute of Experimental Medicine NWB RAMS

D V Sosin

Institute of Experimental Medicine NWB RAMS

D S Penkov

Institute of Experimental Medicine NWB RAMS

S N Proshin

Institute of Experimental Medicine NWB RAMS

P D Shabanov

Institute of Experimental Medicine NWB RAMS

References

  1. Paxinos G. The rat nervous system. — 3d ed. — Amsterdam et al.: Elsevier, 2004. — P. 1176-1780.
  2. Шабанов П.Д., Зарубина И.В., Soultanov V.S. К механизму действия полипренолов при ишемии головного мозга // Мед. акад. журн. — 2011. — Т. 11, № 2. — С. 24-31.
  3. Ginsberg M.D., Busto R. Rodent models of cerebral ischemia // Stroke. — 1989. — Vol. 20. — P. 1627-1642.
  4. Пошивалов В.П. Этологический атлас для фармакологических исследований на лабораторных грызунах. — М., 1978. — Деп. в ВИНИТИ, № 3164-78.
  5. Marysheva V.V., Mikheev V.V., Shabanov P.D. Effect of amtizol on resistance of SHR mice to acute hypoxia with hypercapnia under conditions as isolated functioning of one cerebral hemisphere // Bull. Exp. Biol. Med. — 2013. — Vol. 154, № 4. — P. 453-456.
  6. Васильев Ю.Г., Берестов Д.С. Гомеостаз и пластичность мозга. — Ижевск: Ижевская ГСХА, 2011. — 216 с.
  7. Богомолов Д.В. Судебно-медицинская диагностика наркотической интоксикации по морфологическим данным: автореф. дис.. д-ра мед. наук. — М., 2001. — 29 с.
  8. Дробленков А.В., Карелина Н.Р., Шабанов П.Д. Изменения нейронов и глиоцитов мезоаккумбоцингулярной системы при перинатальном воздействии морфина у крыс // Морфология. — 2009. — Т. 136, № 6. — С. 35-37.
  9. Дробленков А.В. Морфологические признаки отравления этанолом, алкогольной абстиненции и хронической алкогольной интоксикации в мезокортиколимбической дофминергической системе // Суд.-мед. экспертиза. — 2011. — Т. 54, № 5. — С. 11-17.
  10. Okoye G.S., Powel E.M., Geller H.M. Migration of A7 immortalized astrocyte cells grafted into the adult rat striatum // J. Comp. Phys. — 1995. — Vol. 262. — Р. 524-534.
  11. Voskuhl R.R., Peterson R.S., Song B. et al. Reactive astrocytes form scar-like perivascular barriers to leukocytes during adaptive immune inflammation of the CNS // J. Neurosci. — 2009. — Vol. 29. — P. 11511-11522.
  12. Дробленков А.В., Карелина Н.Р. Структурные особенности нейронов и макроглиоцитов взаимосвязанных отделов мезоаккумбоцингулярной дофаминергической системы крыс // Морфология. — 2009. — Т. 136, № 5. — С. 11-17.
  13. Жаботинский Ю.М. Нормальная и патологическая морфология нейрона. — М.: Наука, 1965. — 323 с.
  14. Литвинцев Б.С., Одинак М.М., Гайкова О.Н. и др. Клинико-морфологическая характеристика неврологических проявлений наркомании // Профилактич. и клин. мед. — 2011. — Т. 39, № 2. — С. 99-104.
  15. Гусев Е.И., Скворцова В.И. Ишемия головного мозга. — М.: Медицина, 2001. — 328 с.
  16. Racchetti G., D'Alessandro R., Meldolesi J. Astrocyte stellation, a process dependent on Rac1 is sustained by the regulated exocytosis of enlargeo-somes // Glia. — 2012. — Vol. 60, № 3. — P. 465-475.
  17. Kajihara H., Tsutsumi E., Kinoshita A. еt al. Activated astrocytes with glycogen accumulation in ischemic penumbra during the early stage of brain infarction: immunohistochemical and electron microscopic studies // Brain Res. — 2001. — Vol. 909, № 3. — Р. 92-101.
  18. Charriaut-Marlangue C., Margaill I., Represa A.J. Apoptosis and necrosis after reversible focal ischemia: an in situ DNA fragmentation analysis // Cereb. Blood Flow Metab. — 1996. — Vol. 16. — P. 186-194.

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Copyright (c) 2013 Droblenkov A.V., Naumov N.V., Monid M.V., Sosin D.V., Penkov D.S., Proshin S.N., Shabanov P.D.

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