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Inbred Strains of Mice: SAMP8


Inbr ?+59. Origin: as SAMP1. Albino (c).


Shows accelerated aging (Takeda et al 1991). Deterioration in passive and active avoidance tasks progresses with advancing age and becomes significant at 4 and 8 months of age, respectively (Yagi et al 1988, Ohta et al 1989). Age-related massive occurrence of PAS-positive granular structures often observed in the hippocampus and spongiform degeneration of the reticular formation of the brain stem are unusual neuropathological findings (Akiyama et al 1986). Hippocampal glutamic acid content is higher than in SAMP1 (Nomura et al 1991). Median survivial time is 364 days in conventional conditions.

Akiyama H., Kameyama M., Akiguchi I., Sugiyama H., Kawamata T., Fukuyama H., Kimura H., Matsuchita M., and Takeda T. (1986) Periodic acid-Schiff (PAS)-positive, granular structures increase in the brain of senescence accelerated mouse (SAM). Acta Neuropathol. 72, 124-129. \par

Nomura Y., Kitamura Y., and Zhao X. H. (1991) Aging in the glutamergic 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 (Kameyama T., Domino F., and Nabeshima T., eds), pp. 287-298. NPP Books, Ann Arbor, MI. \par

Ohta A., Hirano T., Yagi H., Tanaka S., Hosokawa M., and Takeda T. (1989) Behavioural characteristics of the SAM-P/8 strain in Sidman active avoidance taks. Brain Res. 498, 195-198. \par

Takeda T., Hosokawa M., and Higuchi K. (1991) Senescence-accelerated mouse (SAM): A novel murine model of accelerated senescence. J. Amer. Geriatr. Soc. 39, 911-919. \par

Yagi H., Katoh S., Akiguchi I., and Takeda T. (1988) Age-related deterioration of ability of aquisition in memory and learning in senescence accelerated mouse: SAM-P/8 as an animal model of disturbances in recent memory. Brain Res. 474, 86-93. \par

Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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