Neuropathological Studies on Strains of Senescence Accelerated Mouse with Age Related Deficits in Learning and Memory

  • Ichiro Akiguchi
  • Hideo Yagi
  • Atsuyoshi Shimada
  • Masaki Ueno
  • Manabu Takemura
  • Takamichi Kitabayashi
  • Naoyuki Seryu
  • Toshio Kawamata
  • Shinichi Nakamura
  • Toshio Takeda
Chapter
Part of the Advances in Behavioral Biology book series (ABBI, volume 44)

Abstract

The senescence-accelerated mouse (SAM) is a murine model of accelerated senescence, which was established by Takeda and colleagues in 1981.1 There are now eight accelerated senescence prone SAMP mice, namely SAMP1, P2, P3, P6, P7, P8, P9 and P10 and three senescence resistant SAMR mice, namely SAMR1, R2 and R4. The latter resistant strains exhibit normal characteristics of aging. In the SAMP series, SAMP8 and SAMP10 show early onset and rapid advancement of senescence, which is revealed by analysis of aging dynamics such as survivorship curve and grading score system.2 They also exhibit a significant age-related deterioration of memory and learning abilities for passive and active avoidance tasks.3,4,5 (Table 1)

Keywords

Brain Atrophy Senile Cataract SAMR Mouse Gracile Nucleus Active Avoidance Task 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in to check access.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    T. Takeda, M. Hosokawa, S. Takeshita, M. Irino, K. Higuchi, T. Matsushita, Y. Tornita, K. Yasuhira, H. Hamamoto, K. Shimizu, M. Ishii, T. Yamamuro, A new mutine model of accelerated senescence, Mech. Aging Dev. 17: 183 (1981).PubMedCrossRefGoogle Scholar
  2. 2.
    M. Hosokawa, R. Kawai, K. Higuchi, S. Takeshita, K. Shimizu, H. Hamamoto, A. Honma, M. Inno, K. Toda, Grading score system; a method for evaluation of the degree of senescence in senescence accelerated mouse (SAM), Mech. Aging Dev. 26: 91 (1984).PubMedCrossRefGoogle Scholar
  3. 3.
    M. Miyamoto, Y. Kiyoto, N. Yamazaki, A. Nagaoka, T. Matsuo, Y. Nagawa, T. Takeda, Age-related changes in learning and memory in the senescence-accelerated mouse (SAM), Physiol. Behay. 38: 399 (1986).CrossRefGoogle Scholar
  4. 4.
    H. Yagi, S. Katoh, I. Akiguchi, et al, Age-related deterioration of ability of acquisition in memory and learning in senescence-accelerated mouse (SAM); SAM P/8 as an animal model of disturbance in recent memory, Brain Res. 474: 86 (1988).PubMedCrossRefGoogle Scholar
  5. 5.
    J. F. Flood, J. E. Morley, Early onset of age-related impairment of aversive and appetitive learning in the SAM-P/8 mouse, J. Gerontol. 47: B52 (1992).PubMedCrossRefGoogle Scholar
  6. 6.
    H. Yagi, M. Inno, T. Matsushita, S. Katoh, M. Umezawa, T. Tsuboyama, M. Hosokawa, I. Akiguchi, R. Tokunaga, T. Takeda, Spontaneous spongiform degeneration of brain stem of senescence accelerated mouse (SAM), J. Neuropathol. Exp. Neurol. 48: 577 (1987).CrossRefGoogle Scholar
  7. 7.
    H. Akiyama, M. Kameyama, I. Akiguchi, H. Sugiyama, T. Kawamata, H. Fukuyama, H. Kimura, M. Matsushita, T. Takeda, Periodic acid-Schiff (PAS)-positive, granular structures increase in the brain of senescence accelerated mouse (SAM), Acta Neuropathol. (Berl.) 72: 124 (1986).CrossRefGoogle Scholar
  8. 8.
    M. Takemura, S. Nakamura, I. Akiguchi, M. Ueno, N. Oka, S. Ishikawa, A. Shimada, J. Kimura, T. Takeda, ß/A4 protein-like immunoreactive granular structures in the brain of senescence-accelerated mouse (SAM), Am. J. Pathol. 142: 1887 (1993).PubMedGoogle Scholar
  9. 9.
    A. Shimada, A. Ohta, I. Akiguchi, T. Takeda, Imbred SAM-P/10 as a mouse model of spontaneous, inherited brain atrophy, J. Neuropathol. Exp. Neurol. 51: 440 (1992).PubMedCrossRefGoogle Scholar
  10. 10.
    A. Shimada, A. Ohta, I. Akiguchi, T. Takeda, Age-related deterioration in conditional avoidance task in the SAM-P/10 mouse; an animal model of spontaneous brain atrophy, Brain Res. 608: 266 (1993).PubMedCrossRefGoogle Scholar
  11. 11.
    A. Shimada, M. Hosokawa, A. Ohta, I. Akiguchi, T. Takeda, Localization of atrophy-prone areas in the aging mouse brain; comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1, Neuroscience (1993) (in press).Google Scholar
  12. 12.
    I. Akiguchi, T. Kawamata, H. Yagi, H. Akiyama, H. Sugiyama, M. Ueno, M. Takemura, M. Tanaka, M. Inno, T. Takeda, Morphological changes of the brain of senescence accelerated mouse (SAM)P/8.;a newly developed memory-deficient strain, in: “Basic, Clinical and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases”, T. Nagatsu, M. Yoshida, and A. Fisher, eds., Vol. 1, Plenum Press, New York (1990).Google Scholar
  13. 13.
    I. Akiguchi, H. Akiyama, H. Sugiyama, T, Kawamata, T. Kimura, H. Yagi, S. Tanaka, M. Inno, T. Takeda, Morphological changes of the brain in senescence accelerated mouse (SAM)-P/8; in: “Proceeding of the first SAM Kyoto Symposium”, T. Takeda, T. Matsuo, I. Akiguchi, eds., The Council for SAM Research, Kyoto (1987).Google Scholar
  14. 14.
    T. Kawamata, S. Nakamura, I. Akiguchi, J.Kimura, M. Kameyama, H. Kimura, T. Takeda, Effect of aging on NADPH-diaphorase neurons in laterodoral tegmental nucleus and striatum of mice, Neurobiol. Aging 11: 185 (1990).PubMedCrossRefGoogle Scholar
  15. 15.
    H. Sugiyama, H. Akiyama, I. Akiguchi, M. Kameyama, T. Takeda, Loss of dendritic spines in hippocampal CAI pyramidal cells of senescence accelerated mouse (SAM); a quantitative Golgi study (Jpn), Clin. Neurol. (Tokyo) 27: 841 (1987).Google Scholar
  16. 16.
    T. Kitabayashi, H. Tomimoto, H. Akiyama, I. Akiguchi, J. Kimura, T. Takeda, Reactive microglia in the brain of senescence-accelerated mouse (SAM); an immunohistochemical study, Can. J. Neurol. Sci. 20 (Supp1.4): 146 (1993).Google Scholar
  17. 17.
    H. Yagi, I. Akiguchi, M. Ueno, M. Takemura, M. Hosokawa, T. Takeda, Quantitative analysis of spongiform degeneration in the brain stem in SAMP8; relationship between spongiform degeneration and age-related deterioration of learning and memory, Biomed. Gerontol. 17; 66 (1993).Google Scholar
  18. 18.
    Y. Nomura, Y. Kitamura, X. H. Zhao, Aging in the glutamatergic system with special reference to the NMDA receptor/ion channel complex in the brains of senescence accelerated mice, in: NMDA receptor related agents, ’Biochemistry, Pharmacology and Behavior“, T. Kameyama, E. F. Domino, eds., NPP Books, Ann Arbor (1991).Google Scholar
  19. 19.
    M. Ueno, I. Akiguchi, H. Naiki, Y. Fujibayashi, H. Fukuyama, J. Kimura, M. Kameyama, T. Takeda, The persistence of high uptake of serum albumin in the olfactory bulbs of mice throughout their adult lives, Arch. Gerontol. Geriatr. 13: 201 (1991).PubMedCrossRefGoogle Scholar
  20. 20.
    M. Ueno, I. Akiguchi, H. Yagi, H. Naiki, Y. Fujibayashi, J. Kimura, T. Takeda, Age related changes in blood-brain barrier: Accelerated deterioration of barrier function in accelerated senescence-prone SAM-P/8 mice with deficit in learning and memory, Arch. Gerontol. Geriatr. 16: 233 (1993).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • Ichiro Akiguchi
    • 1
  • Hideo Yagi
    • 1
  • Atsuyoshi Shimada
    • 2
  • Masaki Ueno
    • 1
  • Manabu Takemura
    • 1
  • Takamichi Kitabayashi
    • 1
  • Naoyuki Seryu
    • 1
  • Toshio Kawamata
    • 1
  • Shinichi Nakamura
    • 1
  • Toshio Takeda
    • 2
  1. 1.Department of NeurologyKyoto UniversityKyoto 606Japan
  2. 2.Department of Senescence BiologyKyoto UniversityKyoto 606Japan

Personalised recommendations