抄録
In Drosophila, age related memory impairment (AMI) of a Pavlovian olfactory association task results from a decrease in amnesiac dependent middle-term memory (MTM). As flies age, their memory retention curves become identical to retention curves of amn mutants. In addition, there is no further decrease in memory upon aging in amn mutants indicating that these mutants are already defective for the memory component lost upon aging. MTM and AMI can be rescued by expression of an amn transgene primarily in DPM neurons which project onto the mushroom bodies. Given that amn mutants resemble aged flies with respect to AMI, it is possible that these mutants age prematurely. However, amn flies actually show a s ignificant extension of lifespan compared to wild type. The extended lifespan of amn is reduced to a normal level when a single copy of an amn transgene is induced, while lifespan is shorter than wild-type when two copies of the transgen e are induced. These results suggest that the amn gene regulates aging in a dose dependent manner. In contrast to long-lived mutants that are defective for insulin-like growth factor signaling (IGF signaling), such as chico and InR, amn mutants have normal body size and weight, and maintain higher locomotor activity and reproductivity even at old age. We are characterizing other memory mutants for lifespan alterations to define a novel interaction between memory, AMI and lifespan.. [Jpn J Physiol 54 Suppl:S227 (2004)]
