Morphological characteristics of the piriform cortex in rats with various neurocognitive disorders after traumatic brain injury
DOI:
https://doi.org/10.26641/1997-9665.2024.3.67-76Keywords:
traumatic brain injury, rats, neurocognitive disorders, piriform cortex, morphology.Abstract
Background. In solving numerous issues related to the treatment and rehabilitation of patients with traumatic brain injury, it is of particular interest to study the pathomorphological mechanisms that determine the nature of the formation and dynamics of neurocognitive disorders at various times after the injury. The study aims to determine the tissue and cellular posttraumatic changes in the structure of the piriform 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 piriform cortex was carried out using the markers β-tubulin, Synaptophysin, GAP43, NCAM1, N-cadherin, GFAP. Results and conclusion. Neurocognitive disorders with memory impairment in the long-term after TBI are accompanied by a deepening of the degeneration of neurocytes of the piriform cortex and the chronicity of neuroinflammation with the activation of the mechanisms of neuronal apoptosis and gliocyte autophagy. The progression of neurodegeneration is accompanied by the activation of microglia and leads to the disintegration and migration of macrogliocytes with the formation of an irreversible mosaic astrocytic deficiency and the formation of glial layers in the form of clutches around hemocapillaries. The preservation of memory function in animals with neurocognitive disorders is associated with the limitation of secondary death of neurocytes and the stabilization of the adhesive properties of astroglia of the piriform cortex, which prevents the formation of astrocytic clutches around newly formed hemocapillaries while maintaining the integrity of the blood-brain barrier. In animals without neurocognitive disorders in the long-term post-traumatic period, compensatory mechanisms in the piriform cortex are implemented through effective neovasculogenesis, limitation of perivascular astrocyte hyperplasia, and neuroinflammation, which prevents neurocyte death and leads to activation of synaptic remodeling.
References
- 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
- 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
- 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
- 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
- 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.
- 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
- 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
- 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
- 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.
- 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.
- 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.
- 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.
- 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
- 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.
- 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.
- 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
- 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
- Bureš J, Burešová O, Huston JP. Techniques and basic experiments for the study of brain and behavior. Second edition. Amsterdam – New York : Elsevier science publishers BV; 2016. 326 p.
- European Convention for the protection of vertebrate animals used for experimental and other scientific purposes. Strasburg : Council of Europe. 1986;123:52.
- 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. Off J Eur Union. 2010;53(L276):33-79.
- Mulish M, Welsh U. (Eds.). Romeis Mikroscopiche technic. Heidelberg : Spektrum Akademischer Verlag; 2010. 551 p. https://doi.org/ 10.1007/978-3-8274-2254-5
- Suvarna SK, Layton C, Bancroft GD. (Eds.). Bancroft's Theory and Practice of Histological Techniques, 8th Edition. Elsevier; 2019. 558 p. https://doi.org/10.1016/B978-0-7020-6864-5.00008-6
- Magaki S, Hojat SA, Wei B, So A, Yong WH. An Introduction to the Performance of Immunohistochemistry. Methods Mol Biol. 2019;1897:289-98. https://doi.org/10.1007/978-1-4939-8935-5_25
- Nguyen T. Immunohistochemistry: A Technical Guide to Current Practices. Cambridge : Cambridge University Press; 2022. 272 p.
- Poslavska, OV. [Determination of linear dimensions and areas of individual morphological objects on photomicrographs using the ImageJ program]. Morphologia. 2016;10(3):377-81.
- Hruzieva TS, Lekhan VM, Ohniev VA, Haliienko LI, Kriachkova LV, Palamar BI. [Biostatistics]. Vinnytsia : New Book; 2020. 384 p.
- 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
- 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
- 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.
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