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Activity‐dependent modulation of K + currents at presynaptic terminals of mammalian central synapses
Author(s) -
Qian Jing,
Saggau Peter
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.1469-7793.1999.0427m.x
Subject(s) - biophysics , chemistry , tetraethylammonium , facilitation , stimulation , extracellular , neuroscience , synapse , channel blocker , electrophysiology , nifedipine , hippocampal formation , neurotransmission , biology , calcium , receptor , biochemistry , potassium , organic chemistry
1 The activity‐dependent regulation of presynaptic K + currents at the CA3‐CA1 synapse in the rat hippocampus was investigated during a train of evoked afferent action potentials. The waveforms of presynaptic compound action potentials (cAPs) and presynaptic Ca 2+ transients ([Ca 2+ ] pre,t ) were measured with fluorescent voltage‐sensitive and Ca 2+ ‐sensitive indicators in rat brain slices. 2 Under control conditions, presynaptic cAPs and the accompanying [Ca 2+ ] pre,t displayed similar amplitudes for each stimulus, suggesting that there was no cumulative change of K + and Ca 2+ currents during the test train. However, when a subgroup of presynaptic K + channels was blocked by a low concentration of 4‐aminopyridine (4‐AP, 40 μ m ), a significant facilitation of the [Ca 2+ ] pre,t was observed. 3 This phenomenon was not due to a direct action of 4‐AP on presynaptic Ca 2+ channels, but to cumulative suppression of the K + conductance as indicated by the corresponding change in waveforms of the cAP and presynaptic fibre volley. The observed facilitation was not an artifact by virtue of increased fibre recruitment, nor was it related to the accumulation of extracellular K + ; rather, it was dependent on Ca 2+ influx and stimulation frequency. The time course of recovery from facilitation was closely related to the decay of the intracellular Ca 2+ concentration. 4 The facilitation was not blocked by a saturating concentration of 4‐AP (8 mM) but was reduced during the application of the K + channel blocker tetraethylammonium (TEA, 10 mM), implicating the involvement of TEA‐sensitive K + channels. Such activity‐dependent suppression of presynaptic K + conductance could lead to excessive transmitter release and might explain the hippocampal epileptiform activity that can be induced by application of 4‐AP.