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Senescence accelerated mice (SAM-P8), which have been established as a model of early senescence, were used for analyses of glutamate decarboxylase 67kDa isoform (GAD67) and extracellular regulated kinase-2 (ERK-2) which were altered by aging. The mice was characterized by neurological abnormal signs such as loss of memory, disorientation and weak response to stimuli, which appeared from 8 to 10 weeks-old. Those neurological disorders might be associated with changes in functions of brain proteins and enzymes regulating metabolic conversion of neurotransmitters and signal transduction. SDS-polyacrylamide gel electrophoresis of proteins in brains of male SAM-P8 showed that alterations in electrophoretic patterns of proteins, which would be involved in the development of brain, according to aging at 8 and 12 weeks in comparison with control mice (SAM-R1) although the alterations were not evidenced in female SAM-P8. Examinations of enzymes of GAD67 and ERK-2 by immunoblotting showed the decrease in their immunoreactivity in male SAM-P8 8 weeks-old, but not in female SAM-P8. These results suggest that the neurological disorder in male SAM-P8 is associated with the impairment of protein biosynthesis for the normal development of brain and with the decrease in enzymes for converting glutamate to gammaaminobutyrate and for signal transduction of the response to stimuli. Furthermore, there are sex differences in the decrease of those enzymes by aging.

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Electrophoretic analyses of glutamate decarboxylase 67 kDa isoform and extracellular regulated kinase isozyme-2 in brains of senescence accelerated mice, SAM-P8.