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Neuroendocrinology Letters incl. Psychoneuroimmunology & Chronobiology

 

Neuroendocrinology Letters incl. Psychoneuroimmunology & Chronobiology,
ISSN 0172–780X Copyright © 2000 Neuroendocrinology Letters

NEL VOL. 22 No. 1
ORIGINAL ARTICLE

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2001; 22:19-26
pii: NEL220101A01
PMID: 11335875

The changes in the ultrastructure of the cerebrovascular junction after traumatic injury of the cerebral cortex in rats
by Michal Walski & Barbara Gajkowska

Keywords:
cerebrovascular junction, trauma, brain macrophages, apoptosis

Abstract:

OBJECTIVES: The effect of the traumatic injury of the cerebral cortex on the ultrastructure of the cerebrovascular junction was studied in rats. The aim of the present study is to describe the ultrastructural alterations in the cerebrovascular junction in rat cerebral cortex after traumatic injury. We were particularly interested in the alterations in endothelium, pericytes and the differentiated population of cerebral macrophages.

MATERIAL AND METHODS: The observations were conducted four days (group I-five animals) and seven days (group II–five animals) after induction of cortical trauma. Traumatic injury was induced in the fronto-temporal region of cerebral cortex in general anesthesia with 20 mg/kg ketamine hydrochloride.


RESULTS: In the first group we found the features of damage of the blood-brain barrier and migration of the morphological blood components to the perivascular space. The trauma caused necrosis and apoptosis within brain tissue. An important observation was the presence of numerous brain macrophages that participated in phagocytosis of damaged cellular elements. Additionally, we found an increase in the connective tissue ground substance around brain capillaries. In the second experimental group we noted an increased number of pericytes (1–3) near capillary walls. In some instances, the basement membrane surrounding the pericytes was interrupted and these cells were also located beyond the rim of the vessel wall. Some pericytes showed numerous phagolysosomes indicating that these cells belonged to perivascular macrophages. Moreover, we observed a population of phagocytes residing in close contact with neurons. These cells were different from the typical perivascular macrophages.


CONCLUSIONS: These observations indicate that the traumatic injury of the brain results in mobilization of a heterogeneous population of brain macrophages. This study indicates that different subpopulations of macrophages emerge in the region of traumatic brain damage, and that the morphology and dynamics of these phagocytes changes and depends on the time elapsed after the initial traumatic incident.

 

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