Age-related deterioration in conditional avoidance task in the SAM-P/10 mouse, an animal model of spontaneous brain atrophy

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice

“…Reportedly, the prefrontal cortex, entorhinal cortex, piriform cortex and striatum are closely interconnected and also connected with the amygdale, which plays a key role in conditioning in rodents. Therefore, they speculated that age-related atrophy in all these structures in SAMP10 mice presumably accounts for the age-related deficits in conditional avoidance learning in this strain of mice [106,107].…”

“…In SAMR1 mice, significant impairment was observed at 23-26 months of age. Thus, the aged SAMP10 mice lost the ability to predict the upcoming electric shock by associating a conditioned stimulus (light) with an unconditioned stimulus [106,107]. Miyamoto [15] investigated the two-way active avoidance response in SAMP10, SAMP8 and SAMR1 mice using a shuttle box.…”

Age-related changes in the brains of senescence-accelerated mice (SAM): Association with glial and endothelial reactions

“…Accelerated-senescence-resistant (SAMR) mice with a normal aging pattern include the SAMR1, -R2, and -R4 strains. Each SAMP strain exhibits a strain-specific and age-related phenotype such as systemic senile amyloidosis (Higuchi et al, 1983), degenerative arthropathy (Chen et al, 1989), senile osteoporosis , senile cataract (Hosokawa et al, 1984), senile thymoma (Hosokawa et al, 1987), deficits in learning and memory (Miyamoto et al, 1986;Shimada et al, 1993;Yagi et al, 1988), and spontaneous brain atrophy (Shimada et al, 1992). These are all known features of human aging (Cotran et al, 1989).…”

Deficiencies of Hippocampal Zn and ZnT3 Accelerate Brain Aging of Rat

“…Shortened life span and early manifestation of various signs of senescence were obtained in prone strains of SAM (SAMP strains) (24), of which P10 strain (SAMP10) shows dysfunction of learning memory and brain atrophy with advancing aging (25,26). Although various attempts have been made to find the mechanism of the deficits in the learning and memory of SAMP10 (25,26), the precise mechanism has not been fully elucidated. Furthermore, in spite of the neurochemical significance of Zn in the process related to learning and memory, there has been no report on the contribution of Zn to the deterioration of learning and memory in SAMP10.…”