Functional Viability: Measurement of Synaptic Vesicle Pool Sizes

Author(s):  
Jana K. Wrosch ◽  
Teja W. Groemer
2016 ◽  
Vol 595 (4) ◽  
pp. 1223-1238 ◽  
Author(s):  
Olusoji A. T. Afuwape ◽  
Catherine R. Wasser ◽  
Thomas Schikorski ◽  
Ege T. Kavalali

2006 ◽  
Vol 96 (4) ◽  
pp. 2025-2033 ◽  
Author(s):  
Court Hull ◽  
Keith Studholme ◽  
Stephen Yazulla ◽  
Henrique von Gersdorff

The number and morphology of synaptic ribbons at photoreceptor and bipolar cell terminals has been reported to change on a circadian cycle. Here we sought to determine whether this phenomenon exists at goldfish Mb-type bipolar cell terminals with the aim of exploring the role of ribbons in transmitter release. We examined the physiology and ultrastructure of this terminal around two time points: midday and midnight. Nystatin perforated-patch recordings of membrane capacitance ( Cm) revealed that synaptic vesicle exocytosis evoked by short depolarizations was reduced at night, even though Ca2+ currents were larger. The efficiency of exocytosis (measured as the Δ Cm jump per total Ca2+ charge influx) was thus significantly lower at night. The paired-pulse ratio remained unchanged, however, suggesting that release probability was not altered. Hence the decreased exocytosis likely reflects a smaller readily releasable vesicle pool at night. Electron microscopy of single sections from intact retinas averaged 65% fewer ribbons at night. Interestingly, the number of active zones did not change from day to night, only the probability of finding a ribbon at an active zone. Additionally, synaptic vesicle halos surrounding the ribbons were more completely filled at night when these on-type bipolar cells are more hyperpolarized. There was no change, however, in the physical dimensions of synaptic ribbons from day to night. These results suggest that the size of the readily releasable vesicle pool and the efficiency of exocytosis are reduced at night when fewer ribbons are present at bipolar cell terminal active zones.


Neuron ◽  
2013 ◽  
Vol 80 (4) ◽  
pp. 934-946 ◽  
Author(s):  
Manjot Bal ◽  
Jeremy Leitz ◽  
Austin L. Reese ◽  
Denise M.O. Ramirez ◽  
Murat Durakoglugil ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Nicolas Michalski ◽  
Juan D Goutman ◽  
Sarah Marie Auclair ◽  
Jacques Boutet de Monvel ◽  
Margot Tertrais ◽  
...  

Hearing relies on rapid, temporally precise, and sustained neurotransmitter release at the ribbon synapses of sensory cells, the inner hair cells (IHCs). This process requires otoferlin, a six C2-domain, Ca2+-binding transmembrane protein of synaptic vesicles. To decipher the role of otoferlin in the synaptic vesicle cycle, we produced knock-in mice (Otof Ala515,Ala517/Ala515,Ala517) with lower Ca2+-binding affinity of the C2C domain. The IHC ribbon synapse structure, synaptic Ca2+ currents, and otoferlin distribution were unaffected in these mutant mice, but auditory brainstem response wave-I amplitude was reduced. Lower Ca2+ sensitivity and delay of the fast and sustained components of synaptic exocytosis were revealed by membrane capacitance measurement upon modulations of intracellular Ca2+ concentration, by varying Ca2+ influx through voltage-gated Ca2+-channels or Ca2+ uncaging. Otoferlin thus functions as a Ca2+ sensor, setting the rates of primed vesicle fusion with the presynaptic plasma membrane and synaptic vesicle pool replenishment in the IHC active zone.


Sign in / Sign up

Export Citation Format

Share Document