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Presynaptic Ca 2+ influx and vesicle exocytosis at the mouse endbulb of Held: a comparison of two auditory nerve terminals
Author(s) -
Lin KunHan,
Oleskevich Sharon,
Taschenberger Holger
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.209189
Subject(s) - free nerve ending , neuroscience , chemistry , exocytosis , electrophysiology , biophysics , vesicle , active zone , neurotransmitter , synaptic vesicle , anatomy , biology , membrane , biochemistry , central nervous system
Non‐technical summary The release of neurotransmitter from presynaptic nerve endings is triggered by Ca 2+ influx through voltage‐gated Ca 2+ 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 Ca 2+ 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 Ca 2+ channels control the release of a single transmitter vesicle at the endbulb of Held.