A quantitative immunocytochemical study of blood-brain barrier to endogenous albumin in cerebral cortex and hippocampus of senescence-accelerated mice (SAM).
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The blood-brain barrier (BBB) to endogenous albumin was studied in the cerebral cortex and hippocampus of the senescence-accelerated prone (SAMP8) mouse and senescence-accelerated resistant (SAMR1) mouse strains in corresponding age groups by using a quantitative immunocytochemical procedure. Brain samples after immersion-fixation were embedded at low temperature in Lowicryl K4M and sectioned with an ultramicrotome. Thin sections were exposed to anti-mouse albumin antiserum followed by protein A-gold. Labeling density (gold particles per microns 2) was recorded over four compartments: vascular lumen, endothelium, subendothelial space, and brain parenchyma (neuropil). Morphometric analysis of the electron micrographs revealed that the barrier function of capillaries located in the cerebral cortex of SAMP8 mice was not significantly different from that in control (SAMR1) mice. Nevertheless, in SAMP8 mice, the percentage of leaking microvessels was higher than in control animals. In the o
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The blood-brain barrier (BBB) to endogenous albumin was studied in the cerebral cortex and hippocampus of the senescence-accelerated prone (SAMP8) mouse and senescence-accelerated resistant (SAMR1) mouse strains in corresponding age groups by using a quantitative immunocytochemical procedure. Brain samples after immersion-fixation were embedded at low temperature in Lowicryl K4M and sectioned with an ultramicrotome. Thin sections were exposed to anti-mouse albumin antiserum followed by protein A-gold. Labeling density (gold particles per microns 2) was recorded over four compartments: vascular lumen, endothelium, subendothelial space, and brain parenchyma (neuropil). Morphometric analysis of the electron micrographs revealed that the barrier function of capillaries located in the cerebral cortex of SAMP8 mice was not significantly different from that in control (SAMR1) mice. Nevertheless, in SAMP8 mice, the percentage of leaking microvessels was higher than in control animals. In the o
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