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Modulation of presynaptic C a 2+ currents in frog motor nerve terminals by high pressure
Author(s) -
Aviner Ben,
Gradwohl Gideon,
Moore Homer J.,
Grossman Yoram
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12267
Subject(s) - chemistry , motor nerve , neurotransmission , biophysics , stimulation , electrophysiology , neuroscience , receptor , biology , biochemistry
Presynaptic C a 2+ ‐dependent mechanisms have already been implicated in depression of evoked synaptic transmission by high pressure ( HP ). Therefore, pressure effects on terminal C a 2+ currents were studied in R ana pipiens peripheral motor nerves. The terminal currents, evoked by nerve or direct stimulation, were recorded under the nerve perineurial sheath with a loose macropatch clamp technique. The combined use of N a + and K + channel blockers, [ C a 2+ ] o changes, voltage‐dependent C a 2+ channel ( VDCC ) blocker treatments and HP perturbations revealed two components of presynaptic C a 2+ currents: an early fast Ca 2+ current ( I CaF ), possibly carried by N ‐type ( C a V 2.2) C a 2+ channels, and a late slow Ca 2+ current ( I CaS ), possibly mediated by L ‐type ( C a V 1) C a 2+ channels. HP reduced the amplitude and decreased the maximum (saturation level) of the C a 2+ currents, I CaF being more sensitive to pressure, and may have slightly shifted the voltage dependence. HP also moderately diminished the N a + action current, which contributed to the depression of VDCC currents. Computer‐based modeling was used to verify the interpretation of the currents and investigate the influence of HP on the presynaptic currents. The direct HP reduction of the VDCC currents and the indirect effect of the action potential decrease are probably the major cause of pressure depression of synaptic release.