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The Journal of Neurophysiology Vol. 87 No. 1 January 2002, pp. 222-228
Copyright ©2002 by the American Physiological Society
Department of Physiology, Faculty of Medicine, Kyoto University, Kyoto 606-8501, Japan
Chuhma, Nao and
Harunori Ohmori.
Role of Ca2+ in the Synchronization of Transmitter
Release at Calyceal Synapses in the Auditory System of Rat. J. Neurophysiol. 87: 222-228, 2002. The
synchronization of transmitter release in the synapse of the medial
nucleus of the trapezoid body (MNTB) is achieved during early postnatal
development as a consequence of elimination of delayed asynchronous
releases and appears to reflect changes in the dynamics of
Ca2+ entry and clearance. To examine the role of
Ca2+ in regulating synchronization of transmitter release
in the mature synapse (after postnatal day 9, P9), we perturbed
Ca2+ dynamics systematically. Replacement of external
Ca2+ (2 mM) with Sr2+ induced delayed
asynchronous release following the major EPSC. We tried to reproduce
asynchronous releases without using Sr2+ and instead by
manipulating the time course and the size of Ca2+ transient
in the presynaptic terminal, under the assumption that replacement of
external Na+ with Li+ or application of eosin-Y
would prolong the lifetime of Ca2+ transient by reducing
the rate of Ca2+ extrusion from the terminal. With
application of Li+, Ca2+ transient in the
terminal was prolonged, the EPSC decay time course was prolonged, and
the EPSC amplitude increased. However, these EPSCs were not followed by
delayed asynchronous release. When Ca2+ influx was reduced,
either by partial Ca2+ channel blockade with a low
concentration of Cd2+ or
-agatoxin IVA, a marked
asynchronous release resulted. This was further enhanced by the
combined application of Li+ or eosin-Y. These results
suggest that cooperative increases of both Ca2+ influx and
Ca2+ clearance capacities leading to a sharper
Ca2+ spike in the presynaptic terminal underlie
synchronized transmitter release in the presynaptic terminal of the MNTB.
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