Genetic and Electrophysiological Investigation of Learning Memory Mechanisms
Final technical rept. 1 May 1997-30 Apr 2000
UTAH UNIV SALT LAKE CITY DEPT OF BIOLOGY
Pagination or Media Count:
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.
- Anatomy and Physiology