Genetic and Electrophysiological Investigation of Learning Memory Mechanisms.

摘要

This research assayed the role of three Drosophila gene products in the synaptic mechanisms of short-term memory: 14-3-3 zeta, origin of replication 3 (ORC3) and alpha-integrin proteins. Null mutation of all three genes result in developmental arrest and lethality, whereas partial loss-of-function mutations cause defects in short-term memory retention in the adult. All three proteins ere found to be localized in presynaptic terminals* specifically associated with presynaptic boutons. Electrophysiological analyses of both null and hypomorphic mutations revealed defects in synaptic transmission. Each class of mutants was defective in presynaptic calcium-dependent neurotransmitter release mechanisms and multiple forms of calcium- and activity-dependent functional presynaptic modulation properties. In particular, all three classes of mutants displayed defective synaptic potentiation following tetanic stimulation (post-tetanic potentiation; tpt). These results suggest that these three gene products play roles in the presynaptic terminal necessary for the synaptic potentiation underlying memory formation.