The antagonistic effects of calcium and potassium on the time course of action of carbamylcholine at the neuromuscular junction

1972 ◽  
Vol 9 (1) ◽  
pp. 319-340 ◽  
Author(s):  
Arthur A. Manthey
1970 ◽  
Vol 56 (3) ◽  
pp. 407-419 ◽  
Author(s):  
Arthur A. Manthey

The rate at which the postjunctional membrane of muscle fibers becomes desensitized to the action of carbamylcholine is increased after the muscle has been soaked in solutions containing increased concentrations of calcium. Some further aspects of this effect of calcium were investigated by measuring changes in the input resistance of single fibers of the frog sartorius during local perfusion of the neuromuscular junction with 2.73 x 10-3 M carbamylcholine in isolated muscles immersed in 165 mM potassium acetate. It was found that (a) sudden changes in the local concentration of calcium brought about by perfusing fibers with carbamylcholine solutions containing 20 mM calcium, 40 mM oxalate, or 40 mM EDTA were followed within 20 sec by marked changes in the rate of desensitization; (b) prior to 13 sec after the introduction of carbamylcholine, however, no effect on the input resistance could be detected even though the muscle had been presoaked in 10 mM calcium; (c) the ability of high concentrations of calcium to bring about rapid desensitization disappears when a lower concentration of carbamylcholine (0.137 x 10-3 M) is applied to the muscle fiber. These findings suggest that calcium present in the extracellular fluid can act directly on the postjunctional membrane to promote the desensitization process and that an increased permeability of the membrane to calcium brought about by the presence of carbamylcholine is a factor which contributes to this action.


Nature ◽  
1968 ◽  
Vol 218 (5147) ◽  
pp. 1178-1179 ◽  
Author(s):  
J. J. REYNOLDS ◽  
J. T. DINGLE
Keyword(s):  

1986 ◽  
Vol 55 (3) ◽  
pp. 484-498 ◽  
Author(s):  
J. M. Wojtowicz ◽  
H. L. Atwood

Synaptic transmission at the neuromuscular junction of the excitatory axon supplying the crayfish opener muscle was examined before and after induction of long-term facilitation (LTF) by a 10-min period of stimulation at 20 Hz. Induction of LTF led to a period of enhanced synaptic transmission, which often persisted for many hours. The enhancement was entirely presynaptic in origin, since quantal unit size and time course were not altered, and quantal content of transmission (m) was increased. LTF was not associated with any persistent changes in action potential or presynaptic membrane potential recorded in the terminal region of the excitatory axon. The small muscle fibers of the walking-leg opener muscle were almost isopotential, and all quantal events could be recorded with an intracellular microelectrode. In addition, at low frequencies of stimulation, m was small. Thus it was possible to apply a binomial model of transmitter release to events recorded from individual muscle fibers and to calculate values for n (number of responding units involved in transmission) and p (probability of transmission for the population of responding units) before and after LTF. In the majority of preparations analyzed (6/10), amplitude histograms of evoked synaptic potentials could be described by a binomial distribution with a small n and moderately high p. LTF produced a significant increase in n, while p was slightly reduced. The results can be explained by a model in which the binomial parameter n represents the number of active synapses and parameter p the mean probability of release at a synapse. Provided that a pool of initially inactive synapses exists, one can postulate that LTF involves recruitment of synapses to the active state.


1997 ◽  
Vol 356 (6) ◽  
pp. 827-837 ◽  
Author(s):  
E. A. van Schaick ◽  
C. Kulkarni ◽  
J. K. von Frijtag Drabbe Künzel ◽  
R. A. A. Mathôt ◽  
G. Cristalli ◽  
...  

1995 ◽  
Vol 89 (s33) ◽  
pp. 50P-50P
Author(s):  
LM Videbæk ◽  
S Kvist ◽  
MJ Mulvany

2010 ◽  
Vol 103 (2) ◽  
pp. 659-666 ◽  
Author(s):  
Xueyong Wang ◽  
Martin J. Pinter ◽  
Mark M. Rich

The Ca2+ dependence of synaptic quantal release is generally thought to be restricted to probability of vesicular release. However, some studies have suggested that the number of release sites ( n) at the neuromuscular junction (NMJ) is also Ca2+ dependent. In this study, we recorded endplate currents over a wide range of extracellular Ca2+ concentrations and found the expected Ca2+ dependency of release. A graphical technique was used to estimate p (probability of release) and n using standard binomial assumptions. The results suggested n was Ca2+ dependent. The data were simulated using compound binomial statistics with variable n (Ca2+ dependent) or fixed n (Ca2+ independent). With fixed n, successful simulation of increasing Ca2+ required that p increase abruptly at some sites from very low to high values. Successful simulation with variable n required the introduction of previously silent release sites ( p = 0) with high values of p. Thus the success of both simulations required abrupt, large increases of p at a subset of release sites with initially low or zero p. Estimates of the time course of release obtained by deconvolving evoked endplate currents with average miniature endplate currents decreased slightly as Ca2+ increased, thus arguing against sequential release of multiple quanta at higher Ca2+ levels. Our results suggest that the apparent Ca2+ dependence of n at the NMJ can be explained by an underlying Ca2+ dependence of a spatially variable p such that p increases abruptly at a subset of sites as Ca2+ is increased.


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