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Presynaptic Ca2+ influx and vesicle exocytosis at the mouse endbulb of Held: A comparison of two auditory nerve terminals.

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Taschenberger,  Holger       
Research Group of Activity-Dependent and Developmental Plasticity at the Calyx of Held, MPI for Biophysical Chemistry, Max Planck Society;

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Citation

Lin, K. H., Oleskevich, S., & Taschenberger, H. (2011). Presynaptic Ca2+ influx and vesicle exocytosis at the mouse endbulb of Held: A comparison of two auditory nerve terminals. The Journal of Physiology, 589(17), 4301-4320. doi:10.1113/jphysiol.2011.209189.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-1C90-4
Abstract
Non-technical summary The release of neurotransmitter from presynaptic nerve endings is triggered by Ca2+ influx through voltage-gated Ca2+ channels (VGCCs) that open when an action potential (AP) invades the presynaptic terminal. The functional properties of VGCCs expressed in presynaptic terminals remain elusive because most terminals are too small to be accessible to electrophysiological recordings. We performed direct presynaptic recordings to characterize Ca2+ channels and transmitter release in a large mammalian presynaptic terminal, the endbulb of Held. Endbulb terminals are formed by the endings of auditory nerve fibres that contact bushy cells located in the anterior ventral cochlear nucleus. We find that endbulb terminals are endowed with >1000 readily releasable vesicles and express an average number of >6000 VGCCs. About half of the VGCCs open during a single AP. Thus, multiple Ca2+ channels control the release of a single transmitter vesicle at the endbulb of Held.