<p>A histological and immunohistochemical analysis (IHC) of the motor cortex and subventricular zone (a neurogenic region) in the right cerebral hemisphere of ICR mice was performed following traumatic brain injury (TBI) induced at the bregma level. Hematoxylin–eosin and cresyl violet staining revealed that TBI causes significant damage to the motor cortex, including tissue edema, neuroinflammation, vascular congestion, cellular and tissue degeneration, disruption of the vascular network, astrolysis, and glial scar formation. Concurrently, the number of neurons in the motor cortex was reduced, while the number of glial cells increased. IHC analysis showed a decreased population of DCX<sup>+</sup> proliferating neuroblasts in the subventricular zone, migration of NeuN<sup>+</sup> neurons from this neurogenic niche toward the injured motor cortex, and impaired migration of GFAP<sup>+</sup> astrocytes. To mitigate neuroinflammation, it is proposed to suppress bone marrow hematopoietic activity and prevent the mobilization of inflammatory cells from the bone marrow into the systemic circulation.</p>

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Histological and Immunohistochemical Analysis of the Mouse Brain Following Traumatic Brain Injury: Identification of Therapeutic Targets and Establishment of Treatment Windows

  • N. N. Ermakova,
  • E. S. Pan,
  • M. A. Zhukova,
  • V. Yu. Pan,
  • I. L. Zharkikh,
  • V. E. Skurikhina,
  • A. M. Dygai

摘要

A histological and immunohistochemical analysis (IHC) of the motor cortex and subventricular zone (a neurogenic region) in the right cerebral hemisphere of ICR mice was performed following traumatic brain injury (TBI) induced at the bregma level. Hematoxylin–eosin and cresyl violet staining revealed that TBI causes significant damage to the motor cortex, including tissue edema, neuroinflammation, vascular congestion, cellular and tissue degeneration, disruption of the vascular network, astrolysis, and glial scar formation. Concurrently, the number of neurons in the motor cortex was reduced, while the number of glial cells increased. IHC analysis showed a decreased population of DCX+ proliferating neuroblasts in the subventricular zone, migration of NeuN+ neurons from this neurogenic niche toward the injured motor cortex, and impaired migration of GFAP+ astrocytes. To mitigate neuroinflammation, it is proposed to suppress bone marrow hematopoietic activity and prevent the mobilization of inflammatory cells from the bone marrow into the systemic circulation.