Abstract
BACKGROUND: Synaptic transmission requires both pre- and post-synaptic elements for neural communication. The postsynaptic structure contributes to the ability of synaptic currents to induce voltage changes in postsynaptic cells. At the Drosophila neuromuscular junction (NMJ), the postsynaptic structure, known as the subsynaptic reticulum (SSR), consists of elaborate membrane folds that link the synaptic contacts to the muscle, but its role in synaptic physiology is poorly understood. RESULTS: In this study, we investigate the role of the SSR with simultaneous intra- and extra-cellular recordings that allow us to identify the origin of spontaneously occurring synaptic events. We compare data from Type 1b and 1s synaptic boutons, which have naturally occurring variations of the SSR, as well as from genetic mutants that up or down-regulate SSR complexity. We observed that some synaptic currents do not result in postsynaptic voltage changes, events we called 'missing quanta'. The frequency of missing quanta is positively correlated with SSR complexity in both natural and genetically-induced variants. Rise-time and amplitude data suggest that passive membrane properties contribute to the observed differences in synaptic effectiveness. CONCLUSION: We conclude that electrotonic decay within the postsynaptic structure contributes to the phenomenon of missing quanta. Further studies directed at understanding the role of the SSR in synaptic transmission and the potential for regulating 'missing quanta' will yield important information about synaptic transmission at the Drosophila NMJ.