The Age-Related Degeneration of Oligodendrocytes in the Hippocampus of the Senescence-Accelerated Mouse (SAM) P8: A Quantitative Immunohistochemical Study

• Published in: Biological & Pharmaceutical Bulletin 2005, Vol.28(4), pp.615-618
• Main Authors: Tanaka, Jun, Okuma, Yasunobu, Tomobe, Koji, Nomura, Yasuyuki
• Format: Article
• Language: English
• Subjects: 2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism; aging; Aging - metabolism; Aging - pathology; Animals; hippocampus; Hippocampus - metabolism; Hippocampus - pathology; Immunohistochemistry; Mice; Mice, Inbred Strains; myelin; Myelin Basic Protein - metabolism; oligodendrocyte; Oligodendroglia - metabolism; Oligodendroglia - pathology; senescence-accelerated mouse (SAM)
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.28.615

The senescence-accelerated mouse (SAM) is known as a murine model for accelerated aging. The SAMP8 shows age-related deficits of learning and memory at an earlier age than control mice (SAMR1). We investigated the changes in oligodendrocytes in the brain of SAMP8, using immunohistochemistry for myelin basic protein (MBP) and 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNP) as an oligodendrocyte marker. SAMP8 at 10 months old showed a decrease in MBP-immunoreactivity (IR) and CNP-IR in the hippocampal CA1 subfield, compared with SAMR1. There were no significant differences in MBP and CNP old in the cerebral cortex and the optic tract between SAMR1 and SAMP8 at 10 months. Furthermore, we measured the area of MBP-IR in the CA1 subfield of both strains and found that the area of MBP-IR in SAMP8 had decreased progressively with age, compared with SAMR1. These results suggest that age-related degeneration of oligodendrocytes had occurred in the hippocampus of SAMP8.