The release of acetylcholine from nerve endings by graded electric pulses

1. The effect of brief depolarizations focally applied to a motor nerve ending was studied. Particular attention was paid to the relation between (i) strength and duration of the pulse and (ii) the size and latency of the resulting end-plate potential. 2. The release of acetylcholine lags behind the depolarization which causes it. If pulses of less than 4 ms duration are used (at 5 °C), the release starts after the end of the pulse. 3. Within a certain range, lengthening the pulse increases the rate of the ensuing transmitter release. 4. Unexpectedly, lengthening the depolarizing pulse also increases the latency of the transmitter release. This finding is discussed in detail. It is regarded as evidence suggesting that entry into the axon membrane of a positively charged substance (external Ca 2+ ions or a calcium compound Ca R + ) is the first step leading to the release of acetylcholine packets from the terminal.

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Role of Ryanodine Receptors in the Effects of Hydrogen Sulfide on Transmitter Release from the Frog Motor Nerve Ending

Bulletin of Experimental Biology and Medicine ◽

10.1007/s10517-013-2067-7 ◽

2013 ◽

Vol 155 (1) ◽

pp. 11-13 ◽

Cited By ~ 10

Author(s):

E. V. Gerasimova ◽

O. V. Yakovleva ◽

A. L. Zefirov ◽

G. F. Sitdikova

Keyword(s):

Hydrogen Sulfide ◽

Nerve Ending ◽

Transmitter Release ◽

Motor Nerve ◽

Ryanodine Receptors ◽

Motor Nerve Ending

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Effects of theophylline and imidazole on the transmitter release from the motor nerve ending facilitated by sodium fluoride

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)59479-3 ◽

1986 ◽

Vol 40 ◽

pp. 244

Author(s):

Toshimi Hattori ◽

Hiroshi Maehashi

Keyword(s):

Sodium Fluoride ◽

Nerve Ending ◽

Transmitter Release ◽

Motor Nerve ◽

Motor Nerve Ending

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Studies in the wave-mechanics of muscle. I. Vibratory motor nerve ending and related radiation patterns of muscular cross striations

American Journal of Anatomy ◽

10.1002/aja.1000580202 ◽

1936 ◽

Vol 58 (2) ◽

pp. 259-311 ◽

Cited By ~ 7

Author(s):

Eben J. Carey

Keyword(s):

Nerve Ending ◽

Motor Nerve ◽

Radiation Patterns ◽

Wave Mechanics ◽

Motor Nerve Ending

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Influence of presynaptic receptors on neuromuscular transmission in rat

AJP Cell Physiology ◽

10.1152/ajpcell.1982.242.5.c366 ◽

1982 ◽

Vol 242 (5) ◽

pp. C366-C372 ◽

Cited By ~ 78

Author(s):

D. F. Wilson

Keyword(s):

Transmitter Release ◽

Action Potentials ◽

Physiological Function ◽

Motor Nerve ◽

Presynaptic Receptors ◽

End Plate ◽

Feedback Pathway ◽

Partial Blockade ◽

Ach Receptors

The presence and physiological significance of acetylcholine (ACh) receptors on motor nerve terminals was examined at the rat diaphragm neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials (EPP), miniature end-plate potentials (MEPP), and resting potentials of the muscle fibers. Muscle action potentials were blocked by the cut-muscle technique. Quantal release was determined by the ratio EPP/MEPP, after correcting for nonlinear summation. Blockade of acetylcholinesterase with eserine and neostigmine was tested to determine the influence of residual ACh on transmitter release. Partial blockade of ACh receptors with curare was examined to further clarify the role of these presynaptic receptors. The experiments demonstrate that residual ACh inhibits transmitter release and that blockade of ACh receptors enhances transmitter release. It is concluded that presynaptic ACh receptors exist and that they serve an important physiological function. It is suggested that the presynaptic ACh receptors normally serve to limit transmitter release in a negative feedback pathway.

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Structural and functional changes of frog neuromuscular junctions in high calcium solutions

Proceedings of the Royal Society of London Series B Biological Sciences ◽

10.1098/rspb.1971.0072 ◽

1971 ◽

Vol 178 (1053) ◽

pp. 407-415 ◽

Cited By ~ 29

Keyword(s):

Transmitter Release ◽

Synaptic Vesicles ◽

Neuromuscular Junctions ◽

Motor Nerve ◽

Secretory Response ◽

Spontaneous Release ◽

Functional Changes ◽

High Calcium ◽

Release Of Acetylcholine ◽

Evoked Transmitter Release

When frog muscles are exposed for several hours to a solution of isotonic calcium chloride, the secretory response of the motor nerve terminals to imposed depolarization ultimately fails and the rate of spontaneous release of acetylcholine also declines towards zero. The failure of depolarization-evoked transmitter release is irreversible while spontaneous release reappears, though in highly abnormal fashion, when the muscle is returned to a normal ionic medium. Examination of motor end-plates, during various stages of calcium treatment, shows that there is gradual intra-axonal agglutination of synaptic vesicles which is only very incompletely reversible. This effect is presumably the consequence of gradual entry and intracellular accumulation of calcium ions. Analogous treatment with isotonic magnesium, while resulting in immediate loss of evoked transmitter release, does not lead to progressive agglutination of synaptic vesicles, nor to irreversible impairment of the secretory response of the nerve terminal. The possible relations between structural and functional changes during calcium and magnesium treatment are discussed.

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Tetrodotoxin and neuromuscular transmission

Proceedings of the Royal Society of London Series B Biological Sciences ◽

10.1098/rspb.1967.0010 ◽

1967 ◽

Vol 167 (1006) ◽

pp. 8-22 ◽

Cited By ~ 89

Keyword(s):

Muscle Fibre ◽

Motor Nerve ◽

Nerve Endings ◽

Applied Current ◽

End Plate ◽

Physiological Properties ◽

Fish Poison ◽

Normal Frequency ◽

Release Of Acetylcholine ◽

Puffer Fish

1. The puffer fish poison, tetrodotoxin ( T . T .) was applied to eliminate impulse propagation in nerve and muscle fibre, and the physiological properties of the neuromuscular junction were studied under this condition. 2. Spontaneous miniature end-plate potentials of normal frequency and amplitude were recorded in the T . T .-paralysed muscle. 3. Depolarization of motor nerve endings by locally applied current still produces the usual increase in the frequency of miniature end-plate potentials (e. p. ps). 4. When brief current pulses are applied to the nerve endings e. p. ps can be evoked, whose size varies with the intensity of the current. The responses are composed, like normal e. p. ps, of a statistically varying number of miniature potentials. The response fails when calcium is removed from the bath. 5. When two identical pulses are applied at varying intervals, facilitation of the second e. p. p. occurs, similar to that observed normally with pairs of nerve impulses. 6. It is concluded that tetrodotoxin while blocking electric excitation in nerve and muscle does not interfere with the release of acetylcholine from nerve endings nor with its local action on the muscle fibre.

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