Dynamics of structural changes in the somatosensory cortex in rats with various neurocognitive disorders after traumatic brain injury

Authors

DOI:

https://doi.org/10.26641/1997-9665.2025.1.35-44

Keywords:

traumatic brain injury, rats, neurocognitive disorders, somatosensory cortex, morphology.

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 microcirculation changes in the post-traumatic period require significant clarification. The study aims to study the tissue and cellular posttraumatic changes in the structure of the somatosensory cortex of rats with various neurocognitive disorders at different times after severe traumatic brain injury. Methods. A "shock acceleration model" was used to reproduce severe traumatic brain injury in rats. According to the results of neurological tests, the rats were divided into three groups: 1) the first – animals after trauma with neurocognitive disorders and memory disorders; 1) the second – animals after trauma with neurocognitive disorders without memory disorders; 3) comparison group – animals after trauma without neurocognitive disorders. A histological, morphometric and immunohistochemical study of the somatosensory cortex was carried out using the markers β-tubulin, Synaptophysin, GAP43, NCAM1, N-cadherin, GFAP. Results. In animals with neurocognitive disorders, a moderate decrease in the total content of neurons of different types in the somatosensory cortex is observed, while in animals without cognitive deficits, the density of neurocytes does not differ from the normal level. The suppressed expression of Synaptophysin in the somatosensory cortex in rats with neurocognitive disorders does not change significantly 20 and 40 days after injury and remains at a low level. In animals of the comparison group, the density of p38-positive synapses is restored during the post-traumatic period. 10 days after injury, in animals of all groups, a moderate accumulation of CD56- and N-cadherin-positive protoplasmic astrocytes in the pericapillary spaces is observed, which is often associated with foci of edema and increased mitotic activity of gliocytes. In animals with neurocognitive disorders, in some cases, astroglia form cell layers on the surface of microvessels in the form of dense couplings, which indicates the blockage of transendothelial transport. 40 days after injury, the number of damaged microvessels with layers of astrocytes on the outer surface is significantly reduced. Conclusion. 10 days after injury, moderately pronounced neurodegenerative and destructive changes occur in the somatosensory cortex due to the post-traumatic cytotoxic cascade. 20 and 40 days after injury, signs of neuroinflammation are reduced regardless of the degree of cognitive deficit.

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. 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 Bi-omed. 2021;34(2):e4438. doi: 10.1002/nbm.4438
  4. Zohar O, Lavy R, Zi X, Nelson TJ, Hongpaisan J, Pick CG, Alkon DL. PKC activa-tor therapeutic for mild traumatic brain injury in mice. Neurobiol Dis 2011;41(2):329-337. DOI: 10.1016/ j.nbd.2010.10.001
  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 reduc-es glial proliferation and scar formation after trau-matic 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 hyper-anxious 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 Respons-es. PLoS One. 2016;11(2):e0149451. DOI: 10.1371/journal.pone.0149451
  9. Shaw BC, Anders VR, Tinkey RA, Habean ML, Brock OD, Frostino BJ, Williams JL. Immunity impacts cognitive deficits across neurological disor-ders. J Neurochem. 2023;10.1111/jnc.15999. doi: 10.1111/jnc.15999.
  10. 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.
  11. 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 con-nectome changes in a rat model of traumatic brain injury. Brain Commun. 2021;3(4):244. doi: 10.1093/braincomms/fcab244.
  12. Griffiths DR, Law LM, Young C, Fuentes A, Truran S, Karamanova N, Bell LC, Turner G, Emer-son H, Mastroeni D, Gonzales RJ, Reaven PD, Quarles CC, Migrino RQ, Lifshitz J. Chron-ic Cognitive and Cerebrovascular Function after Mild Traumatic Brain Injury in Rats. J Neurotrau-ma. 2022;39(19-20):1429-1441. doi: 10.1089/ neu.2022.0015.
  13. Gu YL, Zhang LW, Ma N. Cognitive im-provement of mice induced by exercise prior to traumatic brain injury is associated with cyto-chrome c oxidase. Neurosci Lett. 2014;570:86-91. DOI: 10.1016/ j.neulet.2014.04.004
  14. 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.
  15. Song H, Chen C, Kelley B, Tomasevich A, Lee H, Dolle JP, Cheng J, Garcia B, Meaney DF, Smith DH. Traumatic brain injury recapitulates de-velopmental changes of axons. Prog Neurobiol. 2022;217:102332. doi: 10.1016/j.pneurobio.2022.102332.
  16. 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
  17. 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
  18. Bureš J, Burešová O, Huston JP. Tech-niques and basic experiments for the study of brain and behavior. Second edition. Amsterdam – New York : Elsevier science publishers BV; 2016. 326 p.
  19. European Convention for the protection of vertebrate animals used for experimental and other scientific purposes. Strasburg : Council of Europe. 1986;123:52.
  20. Directive 2010/63/EU of the European Par-liament and of the Council of 22 September 2010 on the Protection of Animals Used for Scientific Purposes. Off J Eur Union. 2010;53(L276):33-79.
  21. Mulish M, Welsh U. (Eds.). Romeis Mikro-scopiche technic. Heidelberg : Spektrum Akad-emischer Verlag; 2010. 551 p. https://doi.org/ 10.1007/978-3-8274-2254-5
  22. Suvarna SK, Layton C, Bancroft GD. (Eds.). Bancroft's Theory and Practice of Histologi-cal Techniques, 8th Edition. Elsevier; 2019. 558 p. https://doi.org/10.1016/B978-0-7020-6864-5.00008-6
  23. Magaki S, Hojat SA, Wei B, So A, Yong WH. An Introduction to the Performance of Im-munohistochemistry. Methods Mol Biol. 2019;1897:289-98. https://doi.org/10.1007/978-1-4939-8935-5_25
  24. Nguyen T. Immunohistochemistry: A Technical Guide to Current Practices. Cambridge : Cambridge University Press; 2022. 272 p.
  25. Poslavska, OV. [Determination of linear dimensions and areas of individual morphological objects on photomicrographs using the ImageJ pro-gram]. Morphologia. 2016;10(3):377-81.
  26. Hruzieva TS, Lekhan VM, Ohniev VA, Ha-liienko LI, Kriachkova LV, Palamar BI. [Biostatis-tics]. Vinnytsia : New Book; 2020. 384 p.
  27. 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):5291-323. doi: 10.1002/cphy.c230007
  28. 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
  29. 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.

Downloads

Published

2025-04-08

How to Cite

Mizyakina , K., Dzyak , L., & Tverdokhlib , I. (2025). Dynamics of structural changes in the somatosensory cortex in rats with various neurocognitive disorders after traumatic brain injury. Морфологія / Morphologia / Morfologìâ, 19(1), 35–44. https://doi.org/10.26641/1997-9665.2025.1.35-44

Issue

Vol. 19 No. 1 (2025)

Section

Статті

License

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

 The authors reserve the right to authorship of their work and transfer to the Journal the right to the first publication of this work under the terms of a license Creative commons Attribution 4.0 International (CC BY 4.0), which allows other people to freely distribute the published work with a mandatory reference to the authors of the original work and the first publication of the work in this journal.
        By submitting a manuscript to the editorial office of the Journal ‘Morphologia’ authors agree to transfer the rights to protect and use the manuscript (all supplemental materials, particularly protected objects such as photos, drawings, diagrams, tables, etc.), including the reproduction in the press and distribution via the Internet; translation of the manuscript into any language; export and import of journal copies with the Authors’ article in order to make it available for public. Authors convey the rights mentioned above to the editorial office without any temporal or territorial limitation all over the world. 
        The Authors guarantee that they have the exclusive rights to use the material transferred to editorial office. Editors are not responsible to third parties for contraventions of warranty given by the Authors. The considered rights are transferred to the editorial office since the moment when the current issue is signed for publishing. Reproduction of materials published in the Journal by other individuals and legal entities is possible only with the consent of Editorial office, with the obligatory indication of the full bibliographic reference of the primary publication. The Authors reserve the right to use the published material, its fragments and parts for teaching materials, oral presentations, dissertation thesis prepararion with obligatory bibliographic citation of the original paper. Electron copy of the published article, downloaded from official journal web-site in .pdf format may be put by authors on the official web-site of their institutions, any other official resources with open access.