Structural and functional transformations of the brain in experimental mild traumatic brain injury



Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

In mild traumatic brain injury, it is of interest to study neurode-generative conditions resulting from inflammatory changes in the nervous tissue. Purpose of the study: in the acute period in case of mild experimental traumatic brain injury, to reveal structural transformations of the nervous tissue of the brain. A modified model of a falling weight was used to reproduce of these trauma in adult rats. An immunohistochemical study of the brain with using rat-specific monoclonal antibodies to endothelin-1, glial fibrillar acidic protein, vimentin, and blood-brain barrier endothelial protein (SMI 71) was performed. It has been established that on the first day after injury in the cerebral cortex of animals, the spasm of blood vessels with capillary ischemia predominates. On day 8, there is an increase in the number of hyper- and hypochromic neurons, and after 14 days, restoration of the tone of the microcircu-latory bed is detected with signs of a violation of the permeability of the blood-brain barrier. A significant redistribution in the tissues of the cerebral hemispheres of glial elements containing acid glial protein and vimentin, as well as neurons producing endothelin-1, was noted. In the delayed post-traumatic period, compensatory reactions of the nervous tissue were revealed, which are characterized by the presence of morphological changes in neurons (an increase in the diameter and number of nucleoli in size) associated with intracellular regeneration, as well as the synthesis of various protein factors in them. Thus, the pathogenesis of mild experimental craniocerebral injury in the ischemic (1 day) and intermediate (8 days) periods is characterized by the presence of mild violations of the structural integrity of the nervous tissue of the brain. In the late post-traumatic period (14 days), neurons and astrocytes exhibit compensatory reactions.

Full Text

Restricted Access

About the authors

N. G Plekhova

Pacific State Medical University

I. V Radkov

Pacific State Medical University

S. V Zinoviev

Pacific State Medical University

V. B Shumatov

Pacific State Medical University

References

  1. Sussman E.S., Pendharkar A.V., Ho A.L. et al. Mild traumatic brain injury and concussion: terminology and classification. Handbook clin. Neurol. 2018; 158: 21-4.
  2. Giza C.C., Hovda D.A. The new neurometabolic cascade of concussion. Neurosurgery 2014; 75(4): 24-33.
  3. Mayer C.L., Huber B.R., Peskind E. Traumatic brain injury, neuroinflammation, and post-traumatic headaches. Headache 2013; 53(9): 1523-30.
  4. Chiu C.C., Liao Y.E., Yang L.Y. et al. Neuroinflammation in animal models of traumatic brain injury. J. Neurosc. Methods 2016; 272: 38-9.
  5. Wang G., Zhang J., Hu X. et al. Microglia/macrophage polarization dynamics in white matter after traumatic brain injury. J. Cereb. Blood Flow Metab. 2013; 33(12): 1864-74.
  6. Masel B.E., De Witt D.S. Traumatic brain injury: A disease process, not an event. J. Neurotrauma 2010; 27(8): 1529-40.
  7. Tobe E.H. Geriatric traumatic brain injury: Relationship to dementia and neurodegenerative disease. J. Gerontol. Geriatr. Res. 2016; 5(2): 1000292.
  8. Mychasiuk R., Farran A., Angoa-Perez M. et al. A novel model of mild traumatic brain injury for juvenile rats. J. Vis. Exp. 2014; 94: 51820.
  9. Антипова М.В., Гусельникова В.В., Коржевский Д.Э. Возрастные особенности структурно-функциональной организации микроглиоцитов стриатума крысы. Мед. акад. журн. 2019; 19(S): 133-4.
  10. Zimatkin S.M., Bon E.I. Dark Neurons of the Brain. Behav. Neurosci. 2018; 48: 908-12.
  11. Safavi F., Li H., Gonnella P. et al. С-kit plays a critical role in induction of intravenous tolerance in experimental autoimmune encephalomyelitis. Immunologic. Research 2015; 61(3): 294-302.
  12. Hua L., Xiao-Qiong W., Min Z. et al. Expression of vimentin and glial fibrillary acidic protein in central nervous system development of rats. Asian Pac. J. Trop. Med. 2017; 10(12): 1185-9.
  13. Sukhorukova E.G., Korzhevskii D.E., Alekseeva O.S. Glial fibrillary acidic protein: The component of iintermediate filaments in the vertebrate brain astrocytes. J. Evol. Biochem. Phys. 2015; 51: 1-10.
  14. Ekmark-Lewen S., Lewen A., Israelsson C. et al. Vimentin and GFAP responses in astrocytes after contusion trauma to the murine brain. Restor. Neurol. Neurosci. 2010; 28(3): 311-21.
  15. Jiang S.X., Slinn J., Aylsworth A. et al. Vimentin participates in microglia activation and neurotoxicity in cerebral ischemia. J. Neurochem. 2012; 122(4): 764-74.
  16. Zamanian J.L., Xu L., Foo L.C. et al. Genomic analysis of reactive astrogliosis. J. Neurosci. 2012; 32(18): 6391-410.
  17. Maegele M., Wafaisade A., Peiniger S. et al. The role of endothelin and endothelin antagonists in traumatic brain injury: a review of the literature. Neurological Research 2011; 33(2): 119-26.

Supplementary files

Supplementary Files
Action
1. JATS XML

Copyright (c) 2022 Eco-Vector



СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: 

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies