scholarly journals Inhibitors of calcium buffering depress evoked transmitter release at the squid giant synapse.

1985 ◽  
Vol 369 (1) ◽  
pp. 145-159 ◽  
Author(s):  
D J Adams ◽  
K Takeda ◽  
J A Umbach
Keyword(s):  
Transmitter Release ◽  
Calcium Buffering ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Evoked Transmitter Release

The effect of repetitive stimulation on the passive electrical properties of the presynaptic terminal of the squid giant synapse

1979 ◽  
Vol 206 (1164) ◽  
pp. 293-306 ◽  
Keyword(s):  
Electrical Properties ◽  
Transmitter Release ◽  
Sea Water ◽  
Presynaptic Terminal ◽  
Repetitive Stimulation ◽  
Constant Current ◽  
Current Pulses ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Passive Electrical Properties

The resting electrical properties of the presynaptic terminal of the squid giant synapse have been determined by using constant current pulses. After short periods of repetitive stimulation, the terminal resistance, time constant and capacitance are found to be increased. These changes are absent in terminals bathed in artificial sea water containing no calcium, and sea water containing 5 mM cobalt. It seems likely that these changes are associated with transmitter release.

scholarly journals Presynaptic potentials and facilitation of transmitter release in the squid giant synapse.

1978 ◽  
Vol 72 (4) ◽  
pp. 487-511 ◽  
Author(s):  
M P Charlton ◽  
G D Bittner
Keyword(s):  
Transmitter Release ◽  
Action Potentials ◽  
Presynaptic Action ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Pulse Stimulation

Presynaptic potentials were studied during facilitation of transmitter release in the squid giant synapse. Changes in action potentials were found to cause some, but not all, of the facilitation during twin-pulse stimulation. During trains of action potentials, there were no progressive changes in presynaptic action potentials which could account for the growth of facilitation. Facilitation could still be detected in terminals which had undergone conditioning depolarization or hyperpolarization. Facilitation could be produced by small action potentials in low [Ca++]o and by small depolarizations in the presence of tetrodotoxin. Although the production of facilitation varied somewhat with presynaptic depolarization, nevertheless, approximately equal amounts of facilitation could be produced by depolarizations which caused the release of very different amounts of transmitter.

Transmitter release induced by injection of calcium ions into nerve terminals

1973 ◽  
Vol 183 (1073) ◽  
pp. 421-425 ◽  
Keyword(s):  
Nerve Terminal ◽  
Calcium Ions ◽  
Transmitter Release ◽  
Nerve Terminals ◽  
Presynaptic Nerve Terminal ◽  
External Fluid ◽  
Giant Synapse ◽  
Evoked Transmitter Release

Calcium ions injected into the presynaptic nerve terminal in the giant synapse of the squid, evoked transmitter release while similar doses of Mg and Mn were ineffective. The transmitter release induced by intracellular application was still observed when Ca was replaced in the external fluid by Mn, in spite of the fact that this abolished transmitter release in response to presynaptic depolarization.

Calcium transients recorded with arsenazo III in the presynaptic terminal of the squid giant synapse

1981 ◽  
Vol 212 (1187) ◽  
pp. 197-211 ◽  
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Sea Water ◽  
Light Signal ◽  
Presynaptic Terminal ◽  
Arsenazo Iii ◽  
Intracellular Ca ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Light Absorbance

Transient changes in free intracellular Ca 2+ concentration were monitored in the presynaptic terminal of the giant synapse of the squid, by means of the Ca 2+ -sensitive dye arsenazo III. Calibration experiments showed a linear relation between the amount of Ca 2+ injected by iontophoresis into the terminal, and the peak size of the arsenazo light absorbance record. A light signal could be detected on tetanic stimulation of the presynaptic axon bathed in sea water containing 45 mm Ca 2+ . During a 1 s tetanus the light signal rose approximately linearly, even though transmitter release declined rapidly and the light signal subsequently declined with a half-time of 2-6 s. The Ca 2+ transient elicited by single nerve impulses was recorded by signal averaging, and showed a time course very much slower than the duration of transmitter release.

scholarly journals Correlation of Transmitter Release with Membrane Properties of the Presynaptic Fiber of the Squid Giant Synapse

1967 ◽  
Vol 50 (11) ◽  
pp. 2579-2601 ◽  
Author(s):  
Kiyoshi Kusano ◽  
David R. Livengood ◽  
Robert Werman
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Membrane Properties ◽  
Ca Current ◽  
Permeability Changes ◽  
Postsynaptic Potential ◽  
Presynaptic Spike ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Tetraethylammonium Ions

Depolarization of the presynaptic terminal by current produced a postsynaptic potential (PSP) which increased with increasing presynaptic polarization and then reached a plateau. Iontophoretic injection of tetraethylammonium ions (TEA) into the presynaptic axon near the terminal produced a prolonged presynaptic spike. The resulting PSP is increased in size and its time course closely followed that of the presynaptic spike. The presynaptic fiber no longer exhibited rectification and strong depolarizations revealed that the PSP reached a maximum with about 110 mv depolarization. Further depolarization produced a decrease in PSP amplitude and finally transmission was blocked. However, a PSP then always appeared on withdrawal of the depolarizing current. Under the conditions of these experiments, the PSP could be considered a direct measure of transmitter release. Bathing the TEA-injected synapse with concentrations of tetrodotoxin (TTX) sufficient to block spike activity in both pre- and postsynaptic axons did not greatly modify postsynaptic electrogenesis. However, doubling TTX concentration reversibly blocked PSP. Thus the permeability changes to Na and K accompanying the spike do not appear necessary for transmitter release. Some other processes related to the level of presynaptic polarization must be involved to explain the data. The inhibition of transmitter release by strong depolarizations appears to be related to Ca action. A membrane Ca current may also be necessary for normal transmitter release.

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