Please use this identifier to cite or link to this item:
Title: Presynaptic nanodomains: A tale of two synapses
Authors: Wang, L.-Y
Augustine, G.J 
Keywords: aequorin
calcium channel
egtazic acid
ethylene glycol 1, 2 bis (2 aminophenyl) ether n, n, n', n' tetraacetic acid
neuronal calcium sensor
potassium channel
unclassified drug
action potential
calcium transport
calyx of Held synapse
cell maturation
excitatory postsynaptic potential
giant axon
mathematical parameters
nerve cell plasticity
neurotransmitter release
presynaptic membrane
protein binding
signal transduction
synapse vesicle
Issue Date: 2015
Citation: Wang, L.-Y, Augustine, G.J (2015). Presynaptic nanodomains: A tale of two synapses. Frontiers in Cellular Neuroscience 8 (JAN) : 1-10. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Here we summarize the evidence from two “giant” presynaptic terminals—the squid giant synapse and the mammalian calyx of Held—supporting the involvement of nanodomain calcium signals in triggering of neurotransmitter release. At the squid synapse, there are three main lines of experimental evidence for nanodomain signaling. First, changing the size of the unitary calcium channel current by altering external calcium concentration causes a non-linear change in transmitter release, while changing the number of open channels by broadening the presynaptic action potential causes a linear change in release. Second, low-affinity calcium indicators, calcium chelators, and uncaging of calcium all suggest that presynaptic calcium concentrations are as high as hundreds of micromolar, which is more compatible with a nanodomain type of calcium signal. Finally, neurotransmitter release is much less affected by the slow calcium chelator, ethylene glycol tetraacetic acid (EGTA), in comparison to the rapid chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid (BAPTA). Similarly, as the calyx of Held synapse matures, EGTA becomes less effective in attenuating transmitter release while the number of calcium channels required to trigger a single fusion event declines. This suggests a developmental transformation of microdomain to nanodomain coupling between calcium channels and transmitter release. Calcium imaging and uncaging experiments, in combination with simulations of calcium diffusion, indicate the peak calcium concentration seen by presynaptic calcium sensors reaches at least tens of micromolar at the calyx of Held. Taken together, data from these provide a compelling argument that nanodomain calcium signaling gates very rapid transmitter release. © 2015 Wang and Augustine.
Source Title: Frontiers in Cellular Neuroscience
ISSN: 16625102
DOI: 10.3389/fncel.2014.00455
Rights: Attribution 4.0 International
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_3389_fncel_2014_00455.pdf1.15 MBAdobe PDF



Google ScholarTM



This item is licensed under a Creative Commons License Creative Commons