Reappearance of miniature endplate potentials in frog neuromuscular junctions “silenced” by lanthanum ions

Neuroscience ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 181-186 ◽  
Author(s):  
M.I. Glavinović ◽  
S. Lee ◽  
R. Miledi
Keyword(s):  
Neuromuscular Junctions ◽  
Lanthanum Ions ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials

4-Aminoquinoline-induced ‘giant’ miniature endplate potentials at mammalian neuromuscular junctions

1982 ◽  
Vol 214 (1195) ◽  
pp. 229-244 ◽  
Keyword(s):  
Nerve Terminal ◽  
Neuromuscular Junctions ◽  
Botulinum Toxin Type A ◽  
Amplitude Distribution ◽  
Botulinum Toxin Type ◽  
Extracellular Potassium ◽  
Coupling Mechanism ◽  
Quantal Acetylcholine Release ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials

4-Aminoquinoline (4-AQ) in concentrations around 200 μM induces, within minutes of its application to isolated mouse or rat neuromuscular junctions, the appearance of a population of miniature endplate potentials (m. e. p. ps) with a larger than normal amplitude, so-called giant m. e. p. ps (g. m. e. p. ps). With amplitudes 21-22 times the modal value of m. e. p. p. amplitude, the population of g. m. e. p. ps. varied between 15 and 45% of the total population of m. e. p. ps. There was no increase in the frequency of m. e. p. ps. but a positive correlation between the frequency of g. m. e. p. ps and the total frequency of m. e. p. ps. In many instances the rise time and decay time of g. m. e. p. ps were prolonged compared to normal. Elevated extracellular calcium concentrations increased the frequency of m. e. p. ps but had no effect on g. m. e. p. p. frequency. High extracellular potassium concentrations markedly increased m. e. p. p. frequency but failed to influence g. m. e. p. p. frequency. Similar observations were made with ethanol 0.1 M, ouabain 200 μM or black widow spider venom. Botulinum toxin type A markedly reduced total m. e. p. p. frequency but 4-AQ still induced g. m. e. p. ps. Nerve stimulation failed to release quanta corresponding to the g. m. e. p. ps. G. m. e. p. ps seemed to originate from quantal acetylcholine release from the nerve terminal since they were abolished by surgical denervation and by the addition of d -tubocurarine to the medium. Blockade of voltage-sensitive calcium or sodium channels by, respectively, manganese ions or tetrodotoxin failed to affect the appear­ance and the frequency of g. m. e. p. ps. The electrophysiological findings and a statistical analysis of the characteristicsofthe m. e. p. psindicatethat they belong to two populations. One population is accelerated by the depolarization–release coupling mechanism responsible for evoked transmitter release and is characterized by an amplitude distribution and a process in time that indicate that they correspond to releases occurring at ' active zones ’ in the nerve terminal. The second population of m. e. p. ps is uninfluenced by nerve terminal depolarization and transmembrane calcium fluxes. This population apparently originates from sites dispersed in the nerve terminal membrane and outside the ‘ active zone ’. 4-AQ increases the frequency of this second m. e. p. p. population without affecting the first population.

Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

1999 ◽  
Vol 81 (3) ◽  
pp. 1428-1431 ◽  
Author(s):  
Hong Cheng ◽  
Michael D. Miyamoto
Keyword(s):  
Nerve Stimulation ◽  
Transmitter Release ◽  
Ringer Solution ◽  
Hypertonic Solution ◽  
Repetitive Nerve Stimulation ◽  
Quantal Transmitter Release ◽  
Before And After ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials ◽  
Made In

Effect of hypertonicity on augmentation and potentiation and on corresponding quantal parameters of transmitter release. Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog ( Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca2+ high Mg2+ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and vars p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n,and p and a marked but transient increase in vars p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for vars p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca2+ influx through voltage-gated calcium channels and that potentiation is due to Na+-induced Ca2+ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release.

The giant miniature endplate potentials frequency is increased in aged rats

2015 ◽  
Vol 584 ◽  
pp. 224-229 ◽  
Author(s):  
Paula A. Pousinha ◽  
Alexandra M. Correia ◽  
Ana M. Sebastião ◽  
Joaquim A. Ribeiro
Keyword(s):  
Aged Rats ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials

Effect of Cooling on Neuromuscular Transmission in the Frog

1958 ◽  
Vol 192 (3) ◽  
pp. 464-470 ◽  
Author(s):  
Choh-Luh Li ◽  
Peter Gouras
Keyword(s):  
Critical Temperature ◽  
Neuromuscular Junction ◽  
Nerve Stimulation ◽  
Neuromuscular Transmission ◽  
The Other ◽  
Sartorius Muscle ◽  
Single Muscle ◽  
Miniature Endplate Potentials ◽  
Endplate Potentials ◽  
Muscle Responses

Recording with intracellular electrodes from endplate regions of frogs sartorius muscle showed that at –1°C miniature endplate potentials still occurred and that the resting membrane potentials differed very little from those recorded at room temperatures. The miniature potentials, however, were decreased in frequency and increased in amplitude by cooling; and at about 5°C, the amplitude began to fall while the frequency continued to be low. It was also at about 5°C that the muscle responses to nerve stimulation frequently consisted of endplate potentials only. Upon rewarming spike potentials again appeared. These observations suggest that there is a critical temperature for neuromuscular transmission, below which impediment of impulse transmission began; and in the frog it is 5°C. The experiments also demonstrated that during the process of cooling a blockage of impulses at one neuromuscular junction and transmission across the other in a single muscle fiber could occur.

Endurance exercise modulates neuromuscular junction of C57BL/6NNia aging mice

1997 ◽  
Vol 83 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Mohamed A. Fahim
Keyword(s):  
Neuromuscular Junction ◽  
Endurance Exercise ◽  
Neuromuscular Junctions ◽  
Safety Margin ◽  
Gluteus Maximus ◽  
Nerve Terminals ◽  
Quantal Content ◽  
Age Related ◽  
Endplate Potentials ◽  
Old Mice

Fahim, Mohamed A. Endurance exercise modulates neuromuscular junction of C57BL/6NNia aging mice. J. Appl. Physiol. 83(1): 59–66, 1997.—The effect of age and endurance exercise on the physiology and morphology of neuromuscular junctions (NMJ) of gluteus maximus muscle was studied in C57BL/6NNia mice. Mice were exercised, starting at 7 or 25 mo of age, at 28 m/min for 60 min/day, 5 days/wk for 12 wk, on a rodent treadmill. Intracellular recordings of spontaneous miniature endplate potentials (MEPP) and the quantal content of endplate potentials (EPP) were recorded from NMJ of 10- and 28-mo-old control and exercised mice. Endurance exercise resulted in significant increases in MEPP amplitudes (23%), quantal content, and safety margin, and a significant decrease in MEPP frequency of young mice, with no change in resting membrane potential or membrane capacitance. Three months of endurance exercise resulted in an increase in MEPP frequency (41%) and decreases in MEPP amplitudes (15%), quantal content, and safety margin of old mice. Endurance exercise resulted in significantly larger nerve terminals (24%) in young animals, suggesting functional adaptation. Nerve terminals in exercised 28-mo-old mice were smaller than in the corresponding control mice, an indication that exercise minimized age-related nerve terminal elaboration. It is concluded that the different physiological responses of young and old gluteus maximus muscles to endurance exercise parallel their morphological responses. This suggests that the mouse NMJ undergoes a process of physiological and morphological remodeling during aging, and such plasticity could be modulated differently by endurance exercise.

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