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1 Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania, School of Medicine, Philadelphia, PA, USA
2 Clinical Studies - New Bolton Center, University of Pennsylvania, School of Veterinary Medicine, Kennett Square, PA, USA
3 Clinical Studies - New Bolton Center, University of Pennsylvania, School of Veterinary Medicine, Kennett Square, PA, USA; Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania, School of Medicine, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: thd{at}vet.upenn.edu.
Hearing requires the hair cell synapse to maintain notable temporal fidelity (1 ms or less) 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, pre-synaptic autoinhibition via metabotropic glutamate receptors, or post-synaptic receptor desensitization. Rather, cochlear hair cell exocytic depression resulted from the exhaustion of a functional vesicle pool. This releasable vesicle pool is large, totaling ~8000 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.
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