Abstract
Synapsins are evolutionarily conserved, highly abundant vesicular phosphoproteins in presynaptic terminals. They are thought to regulate the recruitment of synaptic vesicles from the reserve pool to the readily-releasable pool, in particular when vesicle release is to be maintained at high spiking rates. As regulation of transmitter release is a prerequisite for synaptic plasticity, we use the fruit fly Drosophila to ask whether Synapsin has a role in behavioral plasticity as well; in fruit flies, Synapsin is encoded by a single gene (syn). We tackled this question for associative olfactory learning in larval Drosophila by using the deletion mutant syn(97CS), which had been backcrossed to the Canton-S wild-type strain (CS) for 13 generations. We provide a molecular account of the genomic status of syn(97CS) by PCR and show the absence of gene product on Western blots and nerve-muscle preparations. We found that olfactory associative learning in syn(97CS) larvae is reduced to approximately 50% of wild-type CS levels; however, responsiveness to the to-be-associated stimuli and motor performance in untrained animals are normal. In addition, we introduce two novel behavioral control procedures to test stimulus responsiveness and motor performance after "sham training." Wild-type CS and syn(97CS) perform indistinguishably also in these tests. Thus, larval Drosophila can be used as a case study for a role of Synapsin in associative learning.
