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Facilitation of presynaptic calcium currents in the rat brainstem
Author(s) -
Borst J. G. G.,
Sakmann B.
Publication year - 1998
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.1469-7793.1998.149by.x
Subject(s) - bapta , neuroscience , postsynaptic current , excitatory postsynaptic potential , calcium , neural facilitation , superior olivary complex , postsynaptic potential , chemistry , facilitation , brainstem , biophysics , voltage clamp , voltage dependent calcium channel , electrophysiology , prepulse inhibition , inhibitory postsynaptic potential , biology , cochlear nucleus , medicine , biochemistry , receptor , organic chemistry , schizophrenia (object oriented programming) , psychiatry
1 To study use‐dependent changes in the presynaptic Ca 2+ influx and their contribution to transmitter release, we made simultaneous voltage clamp recordings from presynaptic terminals (the calyces of Held) and postsynaptic cells (the principal cells of the medial nucleus of the trapezoid body) in slices of the rat auditory brainstem. 2 Following a short (2 ms) prepulse to 0 mV, calcium channels opened faster during steps to negative test potentials. During trains of action potential waveforms the Ca 2+ influx per action potential increased. At the same time, however, the amplitude of the EPSCs decreased. 3 The facilitation of the calcium currents appeared to depend on a build‐up of intracellular Ca 2+ , since its magnitude was proportional to the Ca 2+ influx and it was reduced in the presence of 10 m m BAPTA. 4 Facilitation of the presynaptic calcium currents may contribute to short‐term facilitation of transmitter release, observed when quantal output is low. Alternatively, it may counteract processes that contribute to synaptic depression.