Normal functioning of both the CNS and the blood-brain barrier depends on proper functioning of the neurovascular unit (NVU) - a dynamic structure made of neurons, capillary vessel (consisted of endothelial cells, pericytes and basement mebrane), extracellular matrix and vessel-bound astrocytes. Human brain trauma occurs during numerous life-saving neurosurgical procedures (e.g. removal of a brain tumor) associated with disrupted continuity of the meninges followed by interventions within the cerebral parenchyma. Such interventions result in damage to all morphological components of NVU. Our rat model of cerebral cortex injury imitates quite well the respective human neurosurgery situation in that it involves the most typical early and delayed consequences of neurosurgical procedures. This model, enables studying the cortical response to the lesion at cellular and subcellular levels and relating them to the underlying biochemical changes. The injury is being made by excising of a moderate-sized (about 2.5 mm × 2.5 mm × 1.5 mm, length × width × thickness) piece of sensorimotor cortex in the frontotemporal region and resulting in the massive damage of that area. Within first few hours following the lesion the border zone of the damage area showed a perivascular astrocytic edema. Two days after the injury, a massive angiogenesis was observe in this region. Formation of new blood vessels occurred even 30 days after the lesion. Beginning on postinjury day 4, the area around the wound showed an increase in both the number and hypertrophy of astrocytes, that showed an enhance of immunoreactivity for the main astrocytic markers: vimentin and GFAP. Fifth postlesion week a well-formed scar was observed within the operated area. However, 3 months after the operation astrocytic processes began to show an edema, and shortly thereafter the scar presented signs of lysis and dissolution. Beginning 24 hours after the injury, the cortex adjacent to the injury showed the presence of degenerating necrotic and, particularly at later time points, of apoptotic neurons. Our studies reveal that the damage and remodeling of the surgical brain injury zone and its vicinity, as well as forming of the glial scar do not mark an end of the process initiated by the cortical injury. Despite completion of these processes, the area adjacent to the damage was always subject to a secondary damage resulting in brain parenchyma loss that reached far beyond the primary injury zone. Supported by ministry of Scientific research and Information Technology. Project nr N404522838
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