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Sr 2+ ‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro
Author(s) -
Rumpel Eva,
Behrends Jan C.
Publication year - 1999
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 - 10.1111/j.1469-7793.1999.447ae.x
Subject(s) - extracellular , bapta , inhibitory postsynaptic potential , biophysics , chemistry , egta , intracellular , neurotransmission , neuroscience , calcium , biochemistry , biology , receptor , organic chemistry
1 At striatal inhibitory synapses in cell culture, replacement of extracellular Ca 2+ with Sr 2+ desynchronized inhibitory postynaptic currents (IPSCs), reducing their peak amplitude and producing a succession of late, asynchronous synaptic events (late release). In the averaged IPSC waveform this resulted in an increase in both the fast and the slow decay time constant as well as in the time to peak. 2 Rapid removal of extracellular Sr 2+ during late release was without effect on the time course of the averaged IPSC. Thus, late release is not dependent on continuous Sr 2+ influx, but must be related to the way in which Sr 2+ , as opposed to Ca 2+ , interacts with constituents of the intracellular space. 3 After application of the membrane‐permeant acetoxymethyl ester (AM) form of the Ca 2+ ‐chelator BAPTA, Sr 2+ ‐induced late release was greatly reduced and the kinetics of the Sr 2+ ‐dependent IPSC approached those of the Ca 2+ ‐dependent response. EGTA AM had a similar but less pronounced effect. 4 Using rapid solution exchange, we stimulated synapses first in Sr 2+ ‐ or Ca 2+ ‐ and 100–300 ms afterwards in Ca 2+ ‐containing solution. Paired‐pulse facilitation of late release was the same whether the conditioning pulse induced a presynaptic influx of Sr 2+ or of Ca 2+ . 5 It is concluded that Sr 2+ ‐mediated asynchrony is probably due to a less efficient intraterminal buffering of Sr 2+ as opposed to Ca 2+ , allowing for Sr 2+ ions to activate release in an area less confined to the immediate vicinity of the presynaptic Ca 2+ channel. This hypothesis explains both the action of endogenous buffers and the apparent lack of specific facilitatory interaction between Ca 2+ ‐mediated and Sr 2+ ‐induced late release.