What is the possible contribution of Ca2+-stimulated adenylate cyclase to acquisition, consolidation and retention of an associative olfactory memory inDrosophila

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Abstract
We have quantitatively analyzed the effect of the mutationrut, which lesions a Ca2+-stimulated subpopulation (or functional state) of adenylate cyclase, on acquisition, consolidation and retention of an olfactory associative memory inDrosophila. The classical conditioning paradigm developed by Tully and Quinn (1985) was employed. Our data indicate thatrut reduces acquisition and short-term memory in this paradigm, yet does not abolish consolidation of residual memory into an anesthesia-resistant form. Assuming that therut behavioral defect is not due to altered neuroanatomy, the data also suggest that the adenylate cyclase activity lesioned byrut is only one of the molecular processes required for acquisition and short-term memory. These different postulated processes seem to act in parallel but are probably recruited sequentially; the mechanism involvingrut + gene product is necessary for response prior to other mechanisms which do not requirerut +. It is also suggested, on the basis of the present results combined with previous data, that processes which do not require Ca2+-activated cyclase can not fulfill the partial role of this enzyme during acquisition but can partially compensate for its absence in later phases of memory formation.