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.

scholarly journals A quantitative description of stimulation-induced changes in transmitter release at the frog neuromuscular junction.

1982 ◽  
Vol 80 (4) ◽  
pp. 613-638 ◽  
Author(s):  
K L Magleby ◽  
J E Zengel
Keyword(s):  
Transmitter Release ◽  
Neuromuscular Junctions ◽  
Quantitative Description ◽  
Kinetic Properties ◽  
Frog Neuromuscular Junction ◽  
Endplate Potential ◽  
Multiplicative Type ◽  
Induced Changes ◽  
Endplate Potentials ◽  
Frog Sartorius

Endplate potentials were recorded from frog sartorius neuromuscular junctions under conditions of greatly reduced quantal contents to develop a quantitative description of stimulation-induced changes in transmitter release. Four general models relating potentiation, augmentation, and the first and second components of facilitation to transmitter release were developed. These models were then tested by incorporating equations for the kinetic properties of the four components of increased transmitter release and examining the ability of the resulting sets of equations to predict stimulation-induced changes in transmitter release. Three of the models were essentially consistent with the observation that augmentation had a multiplicative type relationship to facilitation. These models could also predict the effect of frequency and duration of stimulation on endplate potential (EPP) amplitude during and after prolonged (40 s) trains including the response to step changes in stimulation rate. These models extend by about two orders of magnitude the duration of stimulation-induced changes in transmitter release that can be accounted for, and show that the combined kinetic properties of potentiation, augmentation, and the two components of facilitation are generally sufficient to account for these changes.

scholarly journals Changes in miniature endplate potential frequency during repetitive nerve stimulation in the presence of Ca2+, Ba2+, and Sr2+ at the frog neuromuscular junction.

1981 ◽  
Vol 77 (5) ◽  
pp. 503-529 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Neuromuscular Junctions ◽  
Fourth Power ◽  
Bathing Solution ◽  
Frog Neuromuscular Junction ◽  
Repetitive Nerve Stimulation ◽  
Time Constants ◽  
Endplate Potential ◽  
Induced Changes

Miniature endplate potentials (MEPPs) were recorded from frog sartorious neuromuscular junctions under conditions of reduced quantal contents to study the effect of repetitive nerve stimulation on asynchronous (tonic) quantal transmitter release. MEPP frequency increased during repetitive stimulation and then decayed back to the control level after the conditioning trains. The decay of the increased MEPP frequency after 100-to 200-impulse conditioning trains can be described by four components that decayed exponentially with time constants of about 50 ms, 500 ms, 7 s, and 80 s. These time constants are similar to those for the decay of stimulation-induced changes in synchronous (phasic) transmitter release, as measured by endplate potential (EPP) amplitudes, corresponding, respectively, to the first and second components of facilitation, augmentation, and potentiation. The addition of small amounts of Ca2+ or Ba2+ to the Ca2+-containing bathing solution, or the replacement of Ca2+ with Sr2+, led to a greater increase in the stimulation-induced increases in MEPP frequency. The Sr-induced increase in MEPP frequency was associated with an increase in the second component of facilitation of MEPP frequency; the Ba-induced increase with an increase in augmentation. These effects of Sr2+ and Ba2+ on stimulation-induced changes in MEPP frequency are similar to the effects of these ions on stimulation-induced changes in EPP amplitude. These ionic similarities and the similar kinetics of decay suggest that stimulation induced changes in MEPP frequency and EPP amplitude have some similar underlying mechanisms. Calculations are presented which show that a fourth power residual calcium model for stimulation-induced changes in transmitter release cannot readily account for the observation that stimulation-induced changes in MEPP frequency and EPP amplitude have similar time-courses.

scholarly journals Role of intracellular Ca2+ in stimulation-induced increases in transmitter release at the frog neuromuscular junction.

1994 ◽  
Vol 104 (2) ◽  
pp. 337-355 ◽  
Author(s):  
J E Zengel ◽  
M A Sosa ◽  
R E Poage ◽  
D R Mosier
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Cyclopiazonic Acid ◽  
Progressive Increase ◽  
Repetitive Stimulation ◽  
Frog Neuromuscular Junction ◽  
Quantal Content ◽  
Carbonyl Cyanide ◽  
Stimulation Of

Under conditions of reduced quantal content, repetitive stimulation of a presynaptic nerve can result in a progressive increase in the amount of transmitter released by that nerve in response to stimulation. At the frog neuromuscular junction, this increase in release has been attributed to four different processes: first and second components of facilitation, augmentation, and potentiation (e.g., Zengel, J. E., and K. L. Magleby. 1982. Journal of General Physiology. 80:583-611). It has been suggested that an increased entry of Ca2+ or an accumulation of intraterminal Ca2+ may be responsible for one or more of these processes. To test this hypothesis, we have examined the role of intracellular Ca2+ in mediating changes in end-plate potential (EPP) amplitude during and after repetitive stimulation at the frog neuromuscular junction. We found that increasing the extracellular Ca2+ concentration or exposing the preparation to carbonyl cyanide m-chlorophenylhydrazone, ionomycin, or cyclopiazonic acid all led to a greater increase in EPP amplitude during conditioning trains of 10-200 impulses applied at a frequency of 20 impulses/s. These experimental manipulations, all of which have been shown to increase intracellular levels of Ca2+, appeared to act by increasing primarily the augmentation component of increased release. The results of this study are consistent with previous suggestions that the different components of increased release represent different mechanisms, and that Ca2+ may be acting at more than one site in the nerve terminal.

scholarly journals Facilitation, augmentation, and potentiation of synaptic transmission at the superior cervical ganglion of the rabbit.

1980 ◽  
Vol 76 (2) ◽  
pp. 213-231 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby ◽  
J P Horn ◽  
D A McAfee ◽  
P J Yarowsky
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Time Constant ◽  
Superior Cervical Ganglion ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Gap Technique ◽  
Cervical Ganglion ◽  
Locke Solution ◽  
Underlying Mechanisms

The effect of repetitive stimulation on synaptic transmission was studied in the isolated superior cervical ganglion of the rabbit under conditions of reduced quantal content. Excitatory postsynaptic potentials (EPSP) were recorded with the sucrose gap technique to obtain estimates of transmitter release. Four components of increased transmitter release, with time constants of decay similar to those observed at the frog neuromuscular junction at 20 degrees C, were found in the ganglion at 34 degrees C: a first component of facilitation, which decayed with a time constant of 59 +/- 14 ms (mean +/- SD); a second component of facilitation, which decayed with a time constant of 388 +/- 97 ms; augmentation, which decayed with a time constant of 7.2 +/- 1 s; and potentiation, which decayed with a time constant of 88 +/- 25 s. The addition of 0.1-0.2 mM Ba2+ to the Locke solution increased the magnitude but not the time constant of decay of augmentation. Ba2+ had little effect on potentiation. The addition of 0.2-0.8 mM Sr2+ to the Locke solution appeared to increase the magnitude of the second component of facilitation. Sr2+ had little effect on augmentation or potentiation. These selective effects of Ba2+ and Sr2+ on the components of increased transmitter release in the rabbit ganglion are similar to the effects of these ions at the frog neuromuscular junction. Although the effects of Ba2+ and Sr2+ are similar in the two preparations, the magnitudes of augmentation and the second component of facilitation after a single impulse were about 6-10 times greater in the rabbit ganglion than at the frog neuromuscular junction. These results suggest that the underlying mechanisms in the nerve terminal that give rise to the components of increased transmitter release in the rabbit ganglion and frog neuromuscular junction are similar but not identical.

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.

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