scholarly journals Differential regulation of evoked and spontaneous neurotransmitter release by C-terminal modifications of complexin

2013 ◽  
Vol 52 ◽  
pp. 161-172 ◽  
Author(s):  
Lauren K. Buhl ◽  
Ramon A. Jorquera ◽  
Yulia Akbergenova ◽  
Sarah Huntwork-Rodriguez ◽  
Dina Volfson ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Differential Regulation

scholarly journals Endogenous tagging reveals differential regulation of Ca2+ channels at single AZs during presynaptic homeostatic potentiation and depression

2017 ◽  
Author(s):  
Scott J. Gratz ◽  
Pragya Goel ◽  
Joseph J. Bruckner ◽  
Roberto X. Hernandez ◽  
Karam Khateeb ◽  
...  
Keyword(s):  
Information Flow ◽  
Neurotransmitter Release ◽  
Synaptic Strength ◽  
Live Imaging ◽  
Differential Regulation ◽  
Synaptic Function ◽  
Homeostatic Plasticity ◽  
Multiple Forms ◽  
Active Zones ◽  
Ca2 Channels

AbstractNeurons communicate through Ca2+-dependent neurotransmitter release at presynaptic active zones (AZs). Neurotransmitter release properties play a key role in defining information flow in circuits and are tuned during multiple forms of plasticity. Despite their central role in determining neurotransmitter release properties, little is known about how Ca2+ channel levels are modulated to calibrate synaptic function. We used CRISPR to tag the Drosophila CaV2 Ca2+ channel Cacophony (Cac) and investigated the regulation of endogenous Ca2+ channels during homeostatic plasticity in males in which all endogenous Cac channels are tagged. We found that heterogeneously distributed Cac is highly predictive of neurotransmitter release probability at individual AZs and differentially regulated during opposing forms of presynaptic homeostatic plasticity. Specifically, Cac levels at AZ are increased during chronic and acute presynaptic homeostatic potentiation (PHP), and live imaging during acute expression of PHP reveals proportional Ca2+ channel accumulation across heterogeneous AZs. In contrast, endogenous Cac levels do not change during presynaptic homeostatic depression (PHD), implying that the reported reduction in Ca2+ influx during PHD is achieved through functional adaptions to pre-existing Ca2+ channels. Thus, distinct mechanisms bi-directionally modulate presynaptic Ca2+ levels to maintain stable synaptic strength in response to diverse challenges, with Ca2+ channel abundance providing a rapidly tunable substrate for potentiating neurotransmitter release over both acute and chronic timescales.

Molecular analysis of neurotransmitter release

1998 ◽  
Vol 33 ◽  
pp. 29-41 ◽  
Author(s):  
Giampietro Schiavo ◽  
Gudrun Stenbeck
Keyword(s):  
Molecular Analysis ◽  
Neurotransmitter Release
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