The Hair Cell Synapse

Author(s):  
Teresa Nicolson
Keyword(s):  
2002 ◽  
Vol 539 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Helen J. Kennedy ◽  
Robert W. Meech

2010 ◽  
Vol 30 (36) ◽  
pp. 12157-12167 ◽  
Author(s):  
J. Zorrilla de San Martin ◽  
S. Pyott ◽  
J. Ballestero ◽  
E. Katz

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Hiu-tung C Wong ◽  
Qiuxiang Zhang ◽  
Alisha J Beirl ◽  
Ronald S Petralia ◽  
Ya-Xian Wang ◽  
...  

Sensory hair cells in the ear utilize specialized ribbon synapses. These synapses are defined by electron-dense presynaptic structures called ribbons, composed primarily of the structural protein Ribeye. Previous work has shown that voltage-gated influx of Ca2+ through CaV1.3 channels is critical for hair-cell synapse function and can impede ribbon formation. We show that in mature zebrafish hair cells, evoked presynaptic-Ca2+ influx through CaV1.3 channels initiates mitochondrial-Ca2+ (mito-Ca2+) uptake adjacent to ribbons. Block of mito-Ca2+ uptake in mature cells depresses presynaptic-Ca2+ influx and impacts synapse integrity. In developing zebrafish hair cells, mito-Ca2+ uptake coincides with spontaneous rises in presynaptic-Ca2+ influx. Spontaneous mito-Ca2+ loading lowers cellular NAD+/NADH redox and downregulates ribbon size. Direct application of NAD+ or NADH increases or decreases ribbon size respectively, possibly acting through the NAD(H)-binding domain on Ribeye. Our results present a mechanism where presynaptic- and mito-Ca2+ couple to confer proper presynaptic function and formation.


2004 ◽  
Vol 91 (6) ◽  
pp. 2422-2428 ◽  
Author(s):  
Marc D. Eisen ◽  
Maria Spassova ◽  
Thomas D. Parsons

Hearing requires the hair cell synapse to maintain notable temporal fidelity (≤1 ms) while sustaining neurotransmitter release for prolonged periods of time (minutes). Here we probed the properties and possible anatomical substrate of prolonged neurotransmitter release by using electrical measures of cell surface area as a proxy for neurotransmitter release to study hair cell exocytosis evoked by repetitive stimuli. We observed marked depression of exocytosis by chick tall hair cells. This exocytic depression cannot be explained by calcium current inactivation, presynaptic autoinhibition by metabotropic glutamate receptors, or postsynaptic receptor desensitization. Rather, cochlear hair cell exocytic depression resulted from the exhaustion of a functional vesicle pool. This releasable vesicle pool is large, totaling approximately 8,000 vesicles, and is nearly 10 times greater than the number of vesicles tethered to synaptic ribbons. Such a large functional pool suggests the recruitment of cytoplasmic vesicles to sustain exocytosis, important for maintaining prolonged, high rates of neural activity needed to encode sound.


2013 ◽  
Vol 521 (14) ◽  
pp. 3260-3271 ◽  
Author(s):  
Albena Kantardzhieva ◽  
M. Charles Liberman ◽  
William F. Sewell

2012 ◽  
Vol 106 (1-2) ◽  
pp. 47-56 ◽  
Author(s):  
Ana Belén Elgoyhen ◽  
Eleonora Katz

2002 ◽  
Vol 5 (2) ◽  
pp. 85-86 ◽  
Author(s):  
Laurence O. Trussell
Keyword(s):  

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