scholarly journals Improved signaling as a result of randomness in synaptic vesicle release

2015 ◽  
Vol 112 (48) ◽  
pp. 14954-14959 ◽  
Author(s):  
Calvin Zhang ◽  
Charles S. Peskin

The probabilistic nature of neurotransmitter release in synapses is believed to be one of the most significant sources of noise in the central nervous system. We show how p0, the probability of release per docked vesicle when an action potential arrives, affects the dynamics of the rate of vesicle release in response to changes in the rate of arrival of action potentials. Furthermore, we examine the theoretical capability of a synapse in the estimation of desired signals using information from the stochastic vesicle release events under the framework of optimal linear filter theory. We find that a small p0, such as 0.1, reduces the error in the reconstruction of the input, or in the reconstruction of the time derivative of the input, from the time series of vesicle release events. Our results imply that the probabilistic nature of synaptic vesicle release plays a direct functional role in synaptic transmission.

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Zhuo Guan ◽  
Monica C Quiñones-Frías ◽  
Yulia Akbergenova ◽  
J Troy Littleton

Synchronous neurotransmitter release is triggered by Ca2+ binding to the synaptic vesicle protein Synaptotagmin 1, while asynchronous fusion and short-term facilitation is hypothesized to be mediated by plasma membrane-localized Synaptotagmin 7 (SYT7). We generated mutations in Drosophila Syt7 to determine if it plays a conserved role as the Ca2+ sensor for these processes. Electrophysiology and quantal imaging revealed evoked release was elevated 2-fold. Syt7 mutants also had a larger pool of readily-releasable vesicles, faster recovery following stimulation, and intact facilitation. Syt1/Syt7 double mutants displayed more release than Syt1 mutants alone, indicating SYT7 does not mediate the residual asynchronous release remaining in the absence of SYT1. SYT7 localizes to an internal membrane tubular network within the peri-active zone, but does not enrich at active zones. These findings indicate the two Ca2+ sensor model of SYT1 and SYT7 mediating all phases of neurotransmitter release and facilitation is not applicable at Drosophila synapses.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Roman M. Lazarenko ◽  
Claire E. DelBove ◽  
Claire E. Strothman ◽  
Qi Zhang

Neuron ◽  
2015 ◽  
Vol 85 (1) ◽  
pp. 6-8 ◽  
Author(s):  
Melissa A. Herman ◽  
Christian Rosenmund

Aging Cell ◽  
2012 ◽  
Vol 11 (3) ◽  
pp. 418-427 ◽  
Author(s):  
Joel M. Rawson ◽  
Tabita Kreko ◽  
Holly Davison ◽  
Rebekah Mahoney ◽  
Alex Bokov ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Eduard Kuriscak ◽  
Petr Marsalek ◽  
Julius Stroffek ◽  
Zdenek Wünsch

Experimental and computational studies emphasize the role of the millisecond precision of neuronal spike times as an important coding mechanism for transmitting and representing information in the central nervous system. We investigate the spike time precision of a multicompartmental pyramidal neuron model of the CA3 region of the hippocampus under the influence of various sources of neuronal noise. We describe differences in the contribution to noise originating from voltage-gated ion channels, synaptic vesicle release, and vesicle quantal size. We analyze the effect of interspike intervals and the voltage course preceding the firing of spikes on the spike-timing jitter. The main finding of this study is the ranking of different noise sources according to their contribution to spike time precision. The most influential is synaptic vesicle release noise, causing the spike jitter to vary from 1 ms to 7 ms of a mean value 2.5 ms. Of second importance was the noise incurred by vesicle quantal size variation causing the spike time jitter to vary from 0.03 ms to 0.6 ms. Least influential was the voltage-gated channel noise generating spike jitter from 0.02 ms to 0.15 ms.


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