Altered Synaptic Plasticity in Drosophila Memory Mutants with a Defective Cyclic AMP Cascade

Abstract

Synaptic transmission was examined in Drosophila mutants deficient in memory function. These mutants, dunce and rutabaga , are defective in different steps of the cyclic adenosine 3′,5′-monophosphate (cAMP) cascade. In both dunce and rutabaga larvae, voltage-clamp analysis of neuromuscular transmission revealed impaired synaptic facilitation and post-tetanic potentiation as well as abnormal responses to direct application of dibutyryl cAMP. In addition, the calcium dependence of transmitter release was shifted in dunce . The results suggest that the cAMP cascade plays a role in synaptic facilitation and potentiation and indicate that synaptic plasticity is altered in Drosophila memory mutants.