Korean J Anat.
2002 Dec;35(6):493-500.
Increased Labelling of Perivascular Phagocytes by Blood Borne HRP in the SAM P10 Brain
- Affiliations
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- 1Department of Anatomy, College of Medicine and Medical Research Institute, Chungbuk National University, Chungbuk, Korea. eylee@med.chungbuk.ac.kr
- 2Department of Pharmacology, College of Medicine and Neuroscience Research Institute, Seoul National University, Seoul, Korea.
Abstract
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The present study examined the uptake of blood borne horseradish peroxidase (HRP) by perivascular cells in the senescence -accelerated mouse prone -10 (SAMP10) and the senescence -accelerated mouse resistant -1 (SAMR1) brains. SAMP10 and SAMR1 brains were studied from mice of each of the following ages: 3 months old SAMP10, 12 ~14 months old SAMP10, 3 months old SAMR1, and 12 ~14 months old SAMR1. Animals were injected via a tail vein with HRP (type VI) solution. Two hours later animals were transcardially perfused with 4% paraformaldehyde and 1% glutaraldehyde mixture. After sectioning with a vibrating microtome, brain sections were stained using a DAB solution. Products of the HRP -DAB reaction were frequently and intensely labelled in the perivascular cells along the microvasculature, especially in the young SAMP10 brain. Electron microscopy revealed that the reaction products were evident in the endothelium of the microvasculature, as well as the perivascular phagocytes of arterioles or venules. In the aged SAMP10, the number of perivascular cells showing HRP -reaction products was lower than in the young SAMP10. Under the electron microscope, the perivascular cells of the aged SAMP10 brain showed very weak intensity of HRP staining, and these cells contained abundant foamy vacuoles or lipid droplets. In both young and aged SAMR1 brains, labelled perivascular phagocytes were very occasionally found. In summary, the present results showed increased uptake of blood -borne HRP by perivascular phagocytes in the young SAMP10 brain, and the age related decrease of this labelling, which suggests altered microvascular barrier function with aging in the SAMP10 brain.