CHANGES OF THE CEREBRAL CORTEX AFTER DOSED TRAUMATIC BRAIN INJURY IN RATS OF DIFFERENT AGES

Abstract

Using dosed lateral fluid percussion, moderate and severe traumatic brain injury (TBI) was modeled in one- and two-yearold rats. Brain sections were stained using the Nissl cresyl violet method and an immunohistochemical reaction was performed for the demonstration of glial fibrillary acidic protein (GFAP), a marker of astrocytes. The results obtained indicate the formation in the cerebral cortex, ipsilateral to the impact, the zones of direct and remote of injury. The zone of direct injury corresponded to the area of immediate contact of the liquid column with the dura mater, whereas the remote area of damage was located laterally and caudally to the former. Morphological signs of the injury depended on the force of impact and were manifested in both age groups by astrocytic gliosis and the thinning of layer I of the cortex resulting from neuronal death. The emergence of ischemia-modified neurons, probably, was due to a local disruption of the blood supply. Disorders in the brain in one-year-old rats had a local character and those in two-year-old rats were diffuse, while gliosis was inhomogeneous. The reproducibility and adequacy of the model allow its use for research of molecular-genetic mechanisms of TBI outcomes in humans, as well as for the identification of common mechanisms of TBI consequences and the pathogenesis of the major diseases, comorbid with TBI, primarily depression and epilepsy.

Keywords

cerebral cortex / neurons / neuroglia / traumatic brain injury / lateral fluid percussion

References

[1] Гехт А. Б., Гуляева Н. В., Крылов В. В. и др. Эпилепсия у больных инсультом и черепно-мозговой травмой. Современная эпилептология. М.: АПКИППРО, 2011. С. 243-251.

[2] Крушинский Л. В. Эволюционно-генетические аспекты поведения. М.: Наука, 1991.

[3] Снесарев П. Е. Общая гистопатология мозговой травмы. М.: Медгиз, 1946.

[4] Carbonell W. S., Grady M. S. Regional and temporal characterization of neuronal, glial, and axonal response after traumatic brain injury in the mouse // Acta Neuropathol. 1999. Vol. 98, № 4. P. 396-406.

[5] Cortez S. C., McIntosh T. K., Noble L. J. Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations // Brain Res. 1989. Vol. 482, № 2. P. 271-282.

[6] D’Ambrosio R., Fender J. S., Fairbanks J. P. et al. Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat // Brain. 2005. Vol. 128, № 1. P. 174-188.

[7] Dawson S. L., Hirsch C. S., Lucas F.V., Sebek B. A. The contrecoup phenomenon. Reappraisal of a classic problem // Hum. Pathol. 1980. Vol. 11, № 2. P. 155-166.

[8] Kabadi S. V., Hilton G. D., Stoica D. A. et al. Fluid-percussion - induced traumatic brain injury model in rats // Nat. Protoc. 2010. Vol. 5, № 6. P. 1552-1563.

[9] LaPlaca M. C., Simon C. M., Prado G. R., Cullen D. K. CNS injury biomechanics and experimental models. // Prog. Brain Res. 2007. Vol. 161. P. 13-26.

[10] McIntosh T. K., Vink R., Noble L. et al. Traumatic brain injury in the rat: characterization of a lateral fluid-percussion model // Neuroscience. 1989. Vol. 28, № 1. P. 233-244.

[11] Oakley R., Tharakan B. Vascular hyperpermeability and aging // Aging Dis. 2014. Vol. 5, № 2. P. 114-125.

[12] O’Connor W. T., Smyth A., Gilchrist M. D. Animal models of traumatic brain injury: a critical evaluation // Pharmacol. Ther. 2011. Vol. 130, № 2. P. 106-113.

[13] Reilly P. The impact of neurotrauma on society: an international perspective // Prog. Brain Res. 2007. Vol. 161. P. 3-9.

[14] Testa J. A., Malec J. F., Moessner A. M., Brown A. W. Outcome after traumatic brain injury: effects of aging on recovery // Arch. Phys. Med. Rehabil. 2005. Vol. 86 № 9. P. 1815-1823.

[15] Thompson H. J., Lifshitz J., Marklund N. et al. Lateral fluid percussion brain injury: a 15-year review and evaluation // J. Neurotrauma. 2005. Vol. 22, № 1. P. 42-75.

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