Immunocytochemical evaluation of the blood-brain barrier to endogenous albumin in the olfactory bulb and pons of senescence-accelerated mice (SAM).

The blood-brain barrier (BBB) to endogenous albumin was studied in the olfactory bulb and pons of the senescence-accelerated prone (SAMP8) mouse and senescence-accelerated resistant (SAMR1) mouse strains by using a quantitative immunocytochemical procedure. Ultrathin sections of Lowicryl K4M-embedded samples were exposed to anti-mouse albumin antiserum followed by protein A-gold. Morphometric analysis of the electron micrographs revealed that in the olfactory bulb of both groups of animals, especially in the internal granular layer, some percentage of capillaries and slightly larger microvessels showed leakage of albumin. However, this percentage was larger in SAMP8 than in SAMR1 mice. In the pons, no significant differences in the permeability of blood microvessels were observed in both groups of mice, although a small fraction of capillaries in SAMP8 mice showed limited extravasation of blood plasma albumin. These observations indicate that the BBB in the olfactory bulb of control and SAMP8 mice is not as tight as it is in the pons or in the previously examined cerebral cortex. The labelling density of the neuropil was slightly higher than in the cerebral cortex, suggesting that albumin may have extravasated locally, in addition to having acces to the parenchyma of the olfactory bulb and pons from neighbouring areas supplied with the non-BBB-type of microvasculature. Furthermore, the data obtained suggest that there is limited (segmental), premature age-related impairment of the BBB function in SAMP8 mice.