Role of Ca2+ in the Synchronization of Transmitter Release at Calyceal Synapses in the Auditory System of Rat

Publisher Website
Google Scholar
Abstract
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 ω-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.