The possible role of fixed membrane surface charges in acetylcholine release at the frog neuromuscular junction

1973 ◽  
Vol 14 (1) ◽  
pp. 365-382 ◽  
Author(s):  
William Van der Kloot ◽  
Hiroshi Kita
Keyword(s):  
Neuromuscular Junction ◽  
Acetylcholine Release ◽  
Membrane Surface ◽  
Frog Neuromuscular Junction ◽  
Surface Charges ◽  
Fixed Membrane

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.

Sign in / Sign up

Export Citation Format

Share Document