Effects of calcium channel blockers on stimulation-induced changes in transmitter release at the frog neuromuscular junction

Synapse ◽  
1993 ◽  
Vol 15 (4) ◽  
pp. 251-262 ◽  
Author(s):  
Janet E. Zengel ◽  
David T. Lee ◽  
Maria A. Sosa ◽  
Dennis R. Mosier
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Channel Blockers ◽  
Induced Changes

Cardiovascular and renal actions of endothelin: effects of calcium-channel blockers

1990 ◽  
Vol 258 (2) ◽  
pp. F254-F258 ◽  
Author(s):  
L. Q. Cao ◽  
R. O. Banks
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Filtration Rate ◽  
Female Rats ◽  
Channel Blockers ◽  
Male And Female ◽  
Pentobarbital Sodium ◽  
Renal Action ◽  
Entire Experiment ◽  
Induced Changes

We have evaluated the effects of two calcium-channel blockers, verapamil (VP) and manganese (Mn), on endothelin (EN)-induced changes in systemic and renal function in pentobarbital sodium-anesthetized female rats and male and female dogs. In the rat studies, saline was infused at 24 microliters/min iv with or without (n = 10) two doses of VP (0.02 mg.kg-1.min-1, n = 5; 0.03 mg.kg-1.min-1, n = 3) or Mn (0.5 mg.kg-1.min-1, n = 5) throughout the entire experiment. After surgery, rats were allowed 60 min to stabilize, and three 20-min control clearances were collected. EN (100 ng.kg-1.min-1) was then added to the infusate for 30 min. EN alone caused an increase in mean arterial pressure (MAP) and a decrease in the glomerular filtration rate (GFR). VP at either dose and Mn totally blocked the EN-induced increase in MAP. However, the two calcium-channel blockers had no effect on the renal action of EN; the GFR (in ml/min) decreased (at 30 min of EN infusion) from 2.7 +/- 0.1 (SE) to 0.7 +/- 0.1 (P less than 0.01) in controls, from 2.5 +/- 0.3 to 0.4 +/- 0.3 with the lower dose of VP (P less than 0.01), from 2.3 +/- 0.1 to 0.6 +/- 0.2 with the higher dose of VP (P less than 0.01), and from 1.5 +/- 0.5 to 0.9 +/- 0.6 with Mn (P less than 0.05). Infusion of EN alone (10 ng.kg-1.min-1, n = 5) and EN with VP (50 micrograms/min, n = 3) into the renal artery of dogs reduced renal blood flow from 3.5 +/- 0.4 to 0.9 +/- 0.2 and from 3.6 +/- 0.6 to 1.2 +/- 0.6 ml.g-1.min-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Diabetes-induced changes in calcium homeostasis and the effects of calcium channel blockers in rat and mice nociceptive neurons

Diabetologia ◽  
2001 ◽  
Vol 44 (10) ◽  
pp. 1302-1309 ◽  
Author(s):  
E. Kostyuk ◽  
N. Voitenko ◽  
I. Kruglikov ◽  
A. Shmigol ◽  
V. Shishkin ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Channel Blockers ◽  
Channel Blockers ◽  
Nociceptive Neurons ◽  
Induced Changes

Calcium channel blockers and transmitter release at the normal human neurornuscular junction

Neurology ◽  
1996 ◽  
Vol 46 (5) ◽  
pp. 1391-1391 ◽  
Author(s):  
D. A. Protti ◽  
R. Reisin ◽  
T. A. Mackinley ◽  
O. D. Uchitel
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Transmitter Release ◽  
Channel Blockers ◽  
Normal Human

scholarly journals Transmitter release is evoked with low probability predominately by calcium flux through single channel openings at the frog neuromuscular junction

2015 ◽  
Vol 113 (7) ◽  
pp. 2480-2489 ◽  
Author(s):  
Fujun Luo ◽  
Markus Dittrich ◽  
Soyoun Cho ◽  
Joel R. Stiles ◽  
Stephen D. Meriney
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Ions ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Vesicle Fusion ◽  
Frog Neuromuscular Junction ◽  
Low Probability ◽  
Presynaptic Calcium

The quantitative relationship between presynaptic calcium influx and transmitter release critically depends on the spatial coupling of presynaptic calcium channels to synaptic vesicles. When there is a close association between calcium channels and synaptic vesicles, the flux through a single open calcium channel may be sufficient to trigger transmitter release. With increasing spatial distance, however, a larger number of open calcium channels might be required to contribute sufficient calcium ions to trigger vesicle fusion. Here we used a combination of pharmacological calcium channel block, high-resolution calcium imaging, postsynaptic recording, and 3D Monte Carlo reaction-diffusion simulations in the adult frog neuromuscular junction, to show that release of individual synaptic vesicles is predominately triggered by calcium ions entering the nerve terminal through the nearest open calcium channel. Furthermore, calcium ion flux through this channel has a low probability of triggering synaptic vesicle fusion (∼6%), even when multiple channels open in a single active zone. These mechanisms work to control the rare triggering of vesicle fusion in the frog neuromuscular junction from each of the tens of thousands of individual release sites at this large model synapse.

Effects of adenosine on Ca2+ entry in the nerve terminal of the frog neuromuscular junction

1999 ◽  
Vol 77 (9) ◽  
pp. 707-714 ◽  
Author(s):  
Richard Robitaille ◽  
Sébastien Thomas ◽  
Milton P Charlton
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Transmitter Release ◽  
Synaptic Depression ◽  
Presynaptic Terminal ◽  
Nerve Terminals ◽  
Frog Neuromuscular Junction ◽  
Induced Changes

This study aimed to test whether nerve-evoked and adenosine-induced synaptic depression are due to reduction in Ca2+ entry in nerve terminals of the frog neuromuscular junction. Nerve terminals were loaded with the fluorescent Ca2+ indicator fluo 3 (fluo 3-AM) or loaded with dextran-coupled Ca2+ green-1 transported from the cut end of the nerve. Adenosine (10-50 µM) did not change the resting level of Ca2+ in the presynaptic terminal, whereas it induced large Ca2+ responses in perisynaptic Schwann cells, indicating that adenosine was active and might have induced changes in the level of Ca2+ in the nerve terminal. Ca2+ responses in nerve terminals could be induced by nerve stimulation (0.5 or 100 Hz for 100 ms) over several hours. In the presence of adenosine (10 µM), the size and duration of the nerve-evoked Ca2+ responses were unchanged. When extracellular Ca2+ concentration was lowered to produce the same reduction in transmitter release as the application of adenosine, Ca2+ responses induced by nerve stimulations were reduced by 40%. This indicates that changes in Ca2+ responsible for the decrease in release should have been detected if the mechanism of adenosine depression involved partial block of Ca2+ influx. Ca2+ responses evoked by prolonged high frequency trains of stimuli (50 Hz for 10 or 30 s), which caused profound depression of transmitter release, were sustained during the whole duration of the stimulation, and adenosine had no effect on these responses. These data indicate that neither adenosine induced synaptic depression nor stimulation-induced synaptic depression are caused by reductions in Ca2+ entry into the presynaptic terminal in the frog neuromuscular junction.Key words: adenosine, Ca2+, nerve terminal, transmitter release, synaptic depression.

scholarly journals Differential effects of Ba2+, Sr2+, and Ca2+ on stimulation-induced changes in transmitter release at the frog neuromuscular junction.

1980 ◽  
Vol 76 (2) ◽  
pp. 175-211 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby
Keyword(s):  
Neuromuscular Junction ◽  
Time Constant ◽  
Transmitter Release ◽  
Repetitive Stimulation ◽  
Kinetic Properties ◽  
Bathing Solution ◽  
Frog Neuromuscular Junction ◽  
Induced Changes ◽  
Endplate Potentials ◽  
Frog Sartorius

Endplate potentials (EPP) were recorded from the frog sartorius neuromuscular junction under conditions of low quantal content to study the effect of Ba2+, Sr2+, and Ca2+ on the changes in evoked transmitter release that occur during and after repetitive stimulation. The addition of 0.1-1 mM Ba2+ or Sr2+ to the Ca2+-containing bathing solution, or the replacement of Ca2+ with 0.8-1.4 mM Sr2+, led to a greater increase in EPP amplitudes during and immediately after repetitive stimulation. These changes in release were analyzed in terms of the four apparent components of increased transmitter release that have previously been distinguished on the basis of their kinetic properties. The Ba2+-induced increase in EPP amplitudes was associated with an increase in the magnitude but not the time constant of decay of augmentation. Ba2+ had little effect on potentiation or the first and second components of facilitation. The Sr2+-induced increase in EPP amplitudes was associated with an increase in the magnitude and the time constant of decay of the second component of facilitation. Sr2+ had little effect on potentiation, augmentation, or the first component of facilitation. The selective effects of Ba2+ on augmentation and of Sr2+ on the second component of facilitation were reversible and could be obtained in the presence of the other ion. The addition of 0.1-0.3 mM Ca2+ to the bathing solution had little effect on potentiation, augmentation, or the two components of facilitation. These results provide pharmacological support for the proposal that there are four different components of increased transmitter release associated with repetitive stimulation and suggest that the underlying factors in the nerve terminal that give rise to these components can act somewhat independently of one another.

Effects of Mg2+on the Stimulation-Induced Changes in Transmitter Release at the Frog Neuromuscular Junction

1995 ◽  
Vol 12 (3) ◽  
pp. 265-270
Author(s):  
Noriko Tanabe ◽  
Akira Morota ◽  
Hiromasa Kijima
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Induced Changes

scholarly journals Effects of Ca2+ channel blockers on transmitter release and presynaptic currents at the frog neuromuscular junction.

1995 ◽  
Vol 486 (3) ◽  
pp. 695-706 ◽  
Author(s):  
E Katz ◽  
P A Ferro ◽  
B D Cherksey ◽  
M Sugimori ◽  
R Llinás ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Channel Blockers ◽  
Presynaptic Currents
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