Brain - Microgliosis

Microgliosis adjacent to an inflammatory mononuclear perivascular cuff (arrow) in a female F344/N rat from a chronic study. Note the many elongated, irregular nuclei of typical microglial cells.
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Nuclei of microglia at a higher magnification in a female F344/N rat from a chronic study. Their elongated irregular nuclear morphology (arrows) is apparent.
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A particularly useful immunohistochemical stain using the Iba-1 antibody to detect these cells (arrows) in the brain in an F344/N rat. Other immunohistochemical methods used as microglial markers include OX-42 and CD68.
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Reactive gliosis and capillary hyperplasia (arrow) in a site of former injury in a female F344/N rat from a chronic study. Capillaries are quickly responsive to injury of adjacent tissue, and endothelial nuclear hypertrophy is evident within 24 hours.
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A mixed gliotic response to injury of the putamen, consisting of reactive astrocytes, macrophages, microglia, and mononuclear cells, in a male B6C3F1 mouse from a chronic study. It is apparent that there is a significant increase in nucleated cells in the region.
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Reactive gemistocytic astrocytosis in a site of healing neural injury stained with hematoxylin and eosin, in a treated female F344/N rat from a chronic study. Note the typical eccentric nucleus and prominent eosinophilic cytoplasm of these reactive astrocytes (arrowheads) and the less frequent micro-binucleate form (arrow).
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comment:
This section deals with the cellular responses of prominent reactive cells in the brain: microglia, capillary endothelial cells, and astrocytes.The microglia are early-responding cells and are apparent in and around an injured site within 12–24 hours. Their evolution to recognizable macrophages is apparent within 48 hours. As macrophages, they have increased cytoplasm, and products of lipid degradation can be detected with periodic acid Schiff reagent and by autofluorescence at 365 nm wavelength. Such phagocytic cells are referred to as lipid phagocytes or, more commonly, “gitter cells.”
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Normal astrocytes, protoplasmic and fibrillary, are diffusely distributed in the nervous system, where they serve, among other functions, to stabilize structure and maintain the neural milieu, neuronal energy processes, and the blood brain barrier. The density of the normal astrocyte population in the brain is increased in the glia limitans just beneath the pia mater, and also around blood vessels.Gemistocytic astrocytosis is an integral part of the progressive response to many forms of neural injury and is helpful in uncovering subtle brain injury, as well as giving an approximation of the chronology of the lesions present. Figure 6

recommendation:
The term “microgliosis” should be used when the preponderance of reactive cells have the typical microglial features mentioned and illustrated above. When the nature of the reactive cells is not clearly apparent, and special techniques to identify the cells are not available, then it is appropriate to use the term Gliosis, NOS (not otherwise specified). Gemistocytic astrocytosis is diagnosed, when present. In focal lesions, the neuroanatomic subsite should be noted. If the lesion is noted in multiple sites, it should be diagnosed as Brain, Microgliosis. In all cases, the lesion should be graded.In the presence of concurrent lesions, lesions with the most severity are typically diagnosed. Other concurrent lesions may be diagnosed separately, if warranted by the severity.
references:
Fix AS, Ross JF, Stitzel SR, Switzer RC. 1996. Integrated evaluation of central nervous system lesions: Stains for neurons, astrocytes, and microglia reveal the spatial and temporal features of MK-801-induced neuronal necrosis in the rat cerebral cortex. Toxicol Pathol 24:291-304. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/8736385
Kimelberg HK. 2010. Functions of mature mammalian astrocytes: A current view. Neuroscientist 16:79-106. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/20236950
Sidoryk-Wegrzynowicz M, Wegrzynowicz M, Lee E, Bowman AB, Aschner M. 2011. Role of astrocytes in brain function and disease. Toxicol Pathol 39:115-123. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/21075920
Web page last updated on: January 02, 2014