Morphological characteristics of the frontal cerebral cortex of rats with various neurocognitive disorders after severe traumatic brain injury

Authors

DOI:

https://doi.org/10.26641/1997-9665.2024.2.55-64

Keywords:

traumatic brain injury, rats, neurocognitive disorders, memory impairment, neurodestruction, frontal cortex, morphometry, immunohistochemical markers.

Abstract

Background. Information about the sensitivity of different neurons and neuroglia cells to injury and their ability to recover depending on the location of the damage and the nature of hemomicrocirculation changes in the post-traumatic period require significant clarification. The aim. Determination of tissue and cellular posttraumatic changes in the structure of the precentral gyrus of the brain frontal lobe of rats with various neurocognitive disorders at different times after severe TBI. Methods. A "shock acceleration model" was used to reproduce severe TBI in rats. According to the results of neurological tests, the rats were divided into three groups: 1) the first – animals after TBI with neurocognitive disorders and memory disorders; 1) the second – animals after TBI with neurocognitive disorders without memory disorders; 3) comparison group – animals after TBI without neurocognitive disorders. A histological, morphometric and immunohistochemical study of the precentral gyrus of the frontal lobe was carried out using the markers β-tubulin, Synaptophysin, GAP43, NCAM1, N-cadherin, GFAP. Results and conclusion. 20 and 40 days after injury, neurons with limited synthetic activity and signs of neurodestruction are stably preserved in the cortex of rats with neurocognitive disorders, regardless of the degree of memory disorders, while in animals without cognitive deficits, damaged neurocytes in the pyramidal layers are not detected. 10 days after severe TBI, significant accumulation of protoplasmic astrocytes in pericapillary spaces is observed in the frontal cortex of animals of all groups, which is often associated with foci of edema and increased mitotic activity of gliocytes. At the same time, large areas of the neuropil with a low density of fibrous astrocytes are formed. After 20 and 40 days of the post-traumatic period, in animals with neurocognitive disorders, foci of astrocytic deficiency persist, in rats of the comparison group, they are very rare. 10 days after severe TBI in animals with neurocognitive disorders, a significant increase in the number of newly formed hemocapillaries with a typical structure is observed. A large number of densely packed protoplasmic astrocytes is found on the surface of damaged capillaries. 40 days after the injury, the number of damaged microvessels with layers of astrocytes on the outer surface significantly decreases. In contrast to these changes, in animals without neurocognitive deficits, the number of damaged microvessels surrounded by astrocytic conglomerates is significantly lower. In animals without neurocognitive disorders, 20 and 40 days after the injury, there is a noticeable reduction in microcirculatory damage.

References

  1. Howlett JR, Nelson LD, Stein MB. Mental Health Consequences of Traumatic Brain Injury. Biol Psychiatry. 2022;91(5):413-420. doi: 10.1016/j.biopsych.2021.09.024.
  2. James SL, Theadom A, Ellenbogen RG. Global, regional, and national burden of traumatic brain injury, 1990-2016 a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019;18(1):56-87. doi: 10.1016/ S1474-4422(18)30415-0.
  3. Zohar O, Lavy R, Zi X, Nelson TJ, Hongpaisan J, Pick CG, Alkon DL. PKC activator therapeutic for mild traumatic brain injury in mice. Neurobiol Dis 2011;41(2):329-337. DOI: 10.1016/j.nbd.2010.10.001
  4. Chary K, Nissi MJ, Nykänen O, Manninen E, Rey RI, Shmueli K, Sierra A, Gröhn O. Quantitative susceptibility mapping of the rat brain after traumatic brain injury. NMR Biomed. 2021;34(2):e4438. doi: 10.1002/nbm.4438.
  5. Wu M, Wang C, Gong Y, Huang Y, Jiang L, Zhang M, Gao R, Dang B. Potential mechanism of TMEM2/CD44 in endoplasmic reticulum stress-induced neuronal apoptosis in a rat model of traumatic brain injury. Int J Mol Med. 2023;52(6):119. doi: 10.3892/ijmm.2023.5322.
  6. Di Giovanni S, Movsesyan V, Ahmed F. Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. Proc Natl Acad Sci USA. 2005;102(23):8333-8338. DOI: 10.1073/pnas.0500989102
  7. Jones NC, Cardamone L, Williams JP, Salzberg MR, Myers D, O'Brien TJ. Experimental traumatic brain injury induces a pervasive hyperanxious phenotype in rats. J Neurotrauma. 2008;25(11):1367-1374. DOI: 10.1089/neu.2008.0641
  8. Bachstetter AD, Zhou Z, Rowe RK. MW151 Inhibited IL-1β Levels after Traumatic Brain Injury with No Effect on Microglia Physiological Responses. PLoS One. 2016;11(2):e0149451. DOI: 10.1371/journal.pone.0149451
  9. Wu W, Tian R, Hao S, Xu F, Mao X, Liu B. A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury. Br J Neurosurg. 2014;28(6):739-745. DOI: 10.3109/02688697.2014.915007
  10. Shaw BC, Anders VR, Tinkey RA, Habean ML, Brock OD, Frostino BJ, Williams JL. Immunity impacts cognitive deficits across neurological disorders. J Neurochem. 2023;10.1111/jnc.15999. doi: 10.1111/jnc.15999.
  11. Nie L, He J, Wang J, Wang R, Huang L, Jia L, Kim YT, Bhawal UK, Fan X, Zille M, Jiang C, Chen X, Wang J. Environmental Enrichment for Stroke and Traumatic Brain Injury: Mechanisms and Translational Implications. Compr Physiol. 2023;14(1):5291-5323. doi: 10.1002/cphy.c230007.
  12. Song H, Chen C, Kelley B, Tomasevich A, Lee H, Dolle JP, Cheng J, Garcia B, Meaney DF, Smith DH. Traumatic brain injury recapitulates developmental changes of axons. Prog Neurobiol. 2022;217:102332. doi: 10.1016/j.pneurobio.2022.102332.
  13. Macks C, Jeong D, Bae S, Webb K, Lee JS. Dexamethasone-Loaded Hydrogels Improve Motor and Cognitive Functions in a Rat Mild Traumatic Brain Injury Model. Int J Mol Sci. 2022;23(19):11153. doi: 10.3390/ijms231911153.
  14. Yang Z, Zhu T, Pompilus M, Fu Y, Zhu J, Arjona K, Arja RD, Grudny MM, Plant HD, Bose P, Wang KK, Febo M. Compensatory functional connectome changes in a rat model of traumatic brain injury. Brain Commun. 2021;3(4):244. doi: 10.1093/braincomms/fcab244.
  15. Gu YL, Zhang LW, Ma N. Cognitive improvement of mice induced by exercise prior to traumatic brain injury is associated with cytochrome c oxidase. Neurosci Lett. 2014;570:86-91. DOI: 10.1016/j.neulet.2014.04.004
  16. Hui Y, Zhao H, Shi L, Zhang H. Traumatic Brain Injury-Mediated Neuroinflammation and Neurological Deficits are Improved by 8-Methoxypsoralen Through Modulating PPARγ/NF-κB Pathway. Neurochem Res. 2023;48(2):625-640. doi: 10.1007/s11064-022-03788-6.
  17. Griffiths DR, Law LM, Young C, Fuentes A, Truran S, Karamanova N, Bell LC, Turner G, Emerson H, Mastroeni D, Gonzales RJ, Reaven PD, Quarles CC, Migrino RQ, Lifshitz J. Chronic Cognitive and Cerebrovascular Function after Mild Traumatic Brain Injury in Rats. J Neurotrauma. 2022;39(19-20):1429-1441. doi: 10.1089/neu.2022.0015.
  18. Marmarou AI, Foda MA, van den Brink W. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 1994;80(2):291-300. doi:10.3171/jns.1994.80.2.0291
  19. Foda MA, Marmarou A. A new model of diffuse brain injury in rats. Part II: Morphological characterization. J Neurosurg. 1994;80(2):301-313. doi:10.3171/jns.1994.80.2.0301
  20. Buresh Ja, Bureshova O, Hyuston DP. Metody i osnovnye eksperimenty po izucheniyu mozga i povedeniya [Methods and basic experiments for the study of the brain and behavior]. Moskva: High school, 1991. 399 p. Russian.
  21. Kaluev AV. Problemy izucheniya stressovogo povedeniya [Problems of studying stress behavior]. Kyiv: CSF, 1999. 132 p. Russian.
  22. Inozemtsev AN, Belnik AP, Ostrovskaya RU. Izucheniye uslovnogo refleksa passivnogo izbeganiya v modifitsirovannoy trekhkamernoy ustanovke. [Study of the conditioned reflex of passive avoidance in a modified three-chamber setup]. Experimental and clinical pharmacology. 2007;70(2):67-69. Russian.
  23. European Convention for the Protection of Vertebrate Animals Used for Experimental and Other Stientific Purposes. Strasburg: Council of Europe. 1986;123:52.
  24. Directive 2010/63/EU of the European Parliament and of the Council of 22 September 2010 on the protection of animals used for scientific purposes. Official Journal of the European Union. 2010;53(L276):33-79.
  25. Poslavska OV. Vyznachennya liniynykh rozmiriv ta ploshch okremykh morfolohichnykh obʺyektiv na mikrofotohrafiyakh za dopomohoyu prohramy ImageJ. [Determination of linear dimensions and areas of individual morphological objects on photomicrographs using the ImageJ program]. Morphologia. 2016;10(3):377-381.

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Published

2024-07-30

How to Cite

Mizyakina , K., & Dzyak , L. (2024). Morphological characteristics of the frontal cerebral cortex of rats with various neurocognitive disorders after severe traumatic brain injury. Морфологія / Morphologia / Morfologìâ, 18(2), 55–64. https://doi.org/10.26641/1997-9665.2024.2.55-64

Issue

Vol. 18 No. 2 (2024)

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