Abstract

Transgenic Tg8 mice provide an experimental model of selective lack of the gene encoding monoamine oxidase A (MAO A), and correspond to analogous human genetic pathology found in a Dutch family. To investigate the possible consequences of the effect of the lack of a major enzyme in serotonin and catecholamine metabolism on cognitive functions, MAO A-deficient mice were subjected to a passive avoidance task. Significant differences in the learning ability and in the retention of passive avoidance response between Tg8 mice and the wild-type mice C3H/HeJ were found. MAO A-deficient mice demonstrated increased step-through latency and a longer retention of memory trace for 11 experimental days as compared to wild-type mice. We found that Tg8 mice are more resistant to detention-induced amnesia and show better social memory in social recognition test than C3H mice. The findings show an enhancement of learning and memory retention in the MAO A-deficient mice.

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