Stimulation of spontaneous transmitter release at the frog neuromuscular junction by 12-O-tetradecanoylphorbol-13-acetate occurs in the absence of extracellular Ca2+ and is enhanced by depolarization

1988 ◽  
Vol 338 (4) ◽  
Author(s):  
P.E. Light ◽  
Z.Y. Sahaf ◽  
S.J. Publicover
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Stimulation Of

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.

Effects of the “calcium ionophore” A-23187 on transmitter release at the frog neuromuscular junction

Life Sciences ◽  
1975 ◽  
Vol 17 (12) ◽  
pp. 1837-1841 ◽  
Author(s):  
Hiroshi Kita ◽  
Kathleen Madden ◽  
William Van der Kloot
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Calcium Ionophore ◽  
Frog Neuromuscular Junction ◽  
A 23187

Intraterminal Ca2+ and Spontaneous Transmitter Release at the Frog Neuromuscular Junction

2001 ◽  
Vol 85 (1) ◽  
pp. 287-294 ◽  
Author(s):  
J. K. Angleson ◽  
W. J. Betz
Keyword(s):  
Neuromuscular Junction ◽  
Phorbol Ester ◽  
Intracellular Recording ◽  
Transmitter Release ◽  
The Other ◽  
Nerve Terminals ◽  
Frog Neuromuscular Junction ◽  
Tetraacetic Acid ◽  
Ratiometric Imaging ◽  
The Relationship

We investigated the relationship between intraterminal Ca2+concentration ([Ca2+]i) and the frequency of miniature end plate potentials (MEPPs) at the frog neuromuscular junction by use of ratiometric imaging of fura-2-loaded nerve terminals and intracellular recording of MEPPs. Elevation of extracellular [KCl] over the range of 2–20 mM resulted in increases in [Ca2+]i and MEPP frequency. Loading terminals with the fast and slow Ca2+-buffers bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid-acetoxymethyl (BAPTA-AM) and EGTA-AM resulted in equivalent reductions in the KCl-dependent increases in MEPP frequency. The [Ca2+]i dependence of MEPP frequency determined by elevation of [Ca2+]i due to application of 0.1–10 μM ionomycin was similar to that determined when [Ca2+]i was raised by increasing extracellular KCl. Measurements in 10 mM extracellular KCl revealed that application of the phorbol ester phorbol 12 myristate 13-acetetate (PMA) caused an increase in MEPP frequency while the inactive analogue, 4α-PMA, did not. PMA application also caused an increase in [Ca2+]i. The relationship between [Ca2+]i and MEPP frequency in PMA was the same as was determined by the other methods of raising [Ca2+]i. Under all conditions tested, our data revealed a low [Ca2+]i threshold for activation of transmitter release and are consistent with a K d for [Ca2+]i on the order of 1 μM.

scholarly journals Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction

2016 ◽  
Vol 7 ◽  
Author(s):  
Eduard Khaziev ◽  
Dmitry Samigullin ◽  
Nikita Zhilyakov ◽  
Nijaz Fatikhov ◽  
Ellya Bukharaeva ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Calcium Signals ◽  
Presynaptic Calcium

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
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