Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0304-3940(99)00967-2
Title: Expression of induced nitric oxide synthase in amoeboid microglia in postnatal rats following an exposure to hypoxia
Authors: You, Y.
Kaur, C. 
Keywords: Amoeboid microglial cells
Blood-brain barrier
Hypoxia
Induced nitric oxide synthase
OX-42
Postnatal rats
Issue Date: 2000
Source: You, Y., Kaur, C. (2000). Expression of induced nitric oxide synthase in amoeboid microglia in postnatal rats following an exposure to hypoxia. Neuroscience Letters 279 (2) : 101-104. ScholarBank@NUS Repository. https://doi.org/10.1016/S0304-3940(99)00967-2
Abstract: The present study showed the expression of induced nitric oxide synthase (iNOS) immunoreactivity in amoeboid microglia following an exposure to transient hypoxia in postnatal rats. iNOS immunoreactivity was expressed mainly in the amoeboid microglia in corpus callosum and subependymal regions of the ventricles within 3 h after hypoxia. The expression declined after 5 h, and became undetectable after 15 h and in longer surviving rats. The immunoreactivity of these cells with OX-42, which is a marker for microglia cells and detects complement type three receptors (CR3), was comparable in the rats exposed to hypoxia and the control rats. Immunoglobulin G (IgG) immunoreactivity was observed in the amoeboid microglia up to 3 h after hypoxia but it was undetectable in longer surviving rats and in the control rats. The iNOS expression in the amoeboid mircoglial cells may be related to the host defense and maintenance of structural integrity of the highly vulnerable periventricular white matter after hypoxia. The immunostaining of amoeboid microglial cells with IgG following hypoxia indicates leakage of plasma immunoglobulin from the blood vessels and its removal by the amoeboid microglial cells. Copyright (C) 2000 Elsevier Science Ireland Ltd.
Source Title: Neuroscience Letters
URI: http://scholarbank.nus.edu.sg/handle/10635/33514
ISSN: 03043940
DOI: 10.1016/S0304-3940(99)00967-2
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