Author: Xiaomin Xing

Publisher:

Published: 2014

Total Pages: 132

ISBN-13:

Ca2+ influx is one of the critical events that trigger synaptic vesicular release, and the accumulation of residual free Ca2+ in synapses is also important for activity-dependent synaptic plasticity. Ca2+ imaging with fluorescence indicators (synthetic or genetically encoded) is a powerful approach to monitor Ca2+ levels in neurons and synapses. Although accumulating studies in vertebrate systems have been carried out to demonstrate the role of Ca2+ in synaptic transmission and plasticity, most of these studies rely on pharmacological methods to infer the molecular mechanism, with less emphasis on forward genetic analysis. The Drosophila neuromuscular junction (NMJ) is a powerful neurogenetic platform for studying synaptic transmission, because of the availability of many mutations. However, not many mutations have been analyzed with Ca2+ imaging. Besides, although Genetically Encoded Ca2+ Indicators (GECIs) including GCaMPs are increasingly popular as the tool to identify neuronal circuits activated by certain stimuli or mediating particular behaviors, the physiological and functional interpretation of neuronal Ca2+ transients reported by GECIs remain obscure. By expressing GCaMPs in NMJ synapses, I characterized a spectrum of genetic mutations including sodium channel alleles parats1, parabss1, potassium channel mutations Shaker (ShM, Sh120), Shab3, ether-a-go-go (eag1, eag4pm), and double mutant eag1 Sh120. Drosophila NMJs contain at least three different types of synapses, which include glutamatergic tonic motor synapse type Ib, phasic motor synapse type Is, and modulatory octopaminergic synapse type II. In this study, I found that the ion channel mutations did not uniformly alter the Ca2+ dynamics in type Ib, Is and II synapses.