Latency of transmitter release at crayfish motor nerve endings examined by intracellular depolarization

1987 ◽  
Vol 65 (1) ◽  
pp. 105-108 ◽  
Author(s):  
J. M. Wojtowicz ◽  
I. Parnas ◽  
H. Parnas ◽  
H. L. Atwood
Keyword(s):  
Transmitter Release ◽  
Sampling Methods ◽  
Procambarus Clarkii ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Quantal Release ◽  
Moderate Size ◽  
Axon Branch ◽  
Individual Motor

Latency of release of individual quanta of transmitter was studied at neuromuscular junctions of a crayfish (Procambarus clarkii). Postsynaptic quantal currents were recorded at individual motor nerve endings with a macropatch electrode while the subterminal axon branch was depolarized by current passed through an intracellular microelectrode. For depolarizing currents of moderate size, the latency of transmitter release did not change when the duration of the depolarizing current was altered. Previous studies in which a contrary result was obtained may have been compromised by artefacts or by the sampling methods employed. The present results do not support the hypothesis of a depolarization-induced "repressor" of quantal release.

Physiological effects of two FMRFamide-related peptides from the crayfish Procambarus clarkii

1995 ◽  
Vol 198 (1) ◽  
pp. 109-116
Author(s):  
M Skerrett ◽  
A Peaire ◽  
P Quigley ◽  
A Mercier
Keyword(s):  
Transmitter Release ◽  
Procambarus Clarkii ◽  
Neuromuscular Junctions ◽  
Input Resistance ◽  
Physiological Effects ◽  
Synaptic Current ◽  
Extensor Muscles ◽  
Neuromuscular Systems ◽  
Dose Dependent ◽  
Measurable Change

The present study examined the effects of two recently identified neuropeptides on crayfish hearts and on neuromuscular junctions of the crayfish deep abdominal extensor muscles. The two peptides, referred to as NF1 (Asn-Arg-Asn-Phe-Leu-Arg-Phe-NH2) and DF2 (Asp-Arg-Asn-Phe-Leu-Arg-Phe-NH2), increased the rate and amplitude of spontaneous cardiac contractions and increased the amplitude of excitatory junctional potentials (EJPs) in the deep extensors. Both effects were dose-dependent, but threshold and EC50 values for the cardiac effects were at least 10 times lower than for the deep extensor effects. The heart responded equally well to three sequential applications of peptide in any given preparation, but the responses of the deep extensors appeared to decline with successive peptide applications. The results support the hypothesis that these two neuropeptides act as neurohormones to modulate the cardiac and neuromuscular systems in crayfish. Quantal synaptic current recordings from the deep extensor muscles indicate that both peptides increase the number of quanta of transmitter released from synaptic terminals. Neither peptide elicited a measurable change in the size of quantal synaptic currents. NF1 caused a small increase in muscle cell input resistance, while DF2 did not alter input resistance. These data suggest that DF2 increases EJP amplitudes primarily by increasing transmitter release, while the increase elicited by NF1 appears to involve presynaptic and postsynaptic mechanisms.

Transmitter release induced by a ‘factor’ in rabbit serum

1974 ◽  
Vol 187 (1087) ◽  
pp. 235-241 ◽  
Keyword(s):  
Complement System ◽  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Rabbit Serum ◽  
Nerve Terminals ◽  
The Complement System ◽  
The Way

Non-heated rabbit serum causes massive transmitter release from motor nerve endings. The effect is not observed after heating the serum, in the way usually done to destroy complement. It seems that serum may be acting on the nerve terminals by a mechanism involving the complement system in the absence of antibody.

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

1971 ◽  
Vol 178 (1053) ◽  
pp. 407-415 ◽  
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.

Two-component action of ATP on transmitter release from the motor nerve endings at the neuromuscular junction

2006 ◽  
Vol 99 (2-3) ◽  
pp. 1
Author(s):  
Rachid Giniatullin ◽  
Serguey Grishin ◽  
Arthur Giniatullin
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Two Component

Muscarinic agonists have no effect on spontaneous quantum transmitter release from frog motor nerve endings

1987 ◽  
Vol 103 (2) ◽  
pp. 207-209
Author(s):  
E. E. Nikol'skii ◽  
�. A. Bukharaeva
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Muscarinic Agonists

Extra- and Intracellular Sphingosylphosphorylcholine Promote Spontaneous Transmitter Release from Frog Motor Nerve Endings

2003 ◽  
Vol 63 (6) ◽  
pp. 1430-1436 ◽  
Author(s):  
Eugen Brailoiu ◽  
Nae J. Dun
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings

scholarly journals 4-AMINOPYRIDINE AND EVOKED TRANSMITTER RELEASE FROM MOTOR NERVE ENDINGS

1978 ◽  
Vol 64 (4) ◽  
pp. 623-629 ◽  
Author(s):  
P. ILLES ◽  
S. THESLEFF
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Evoked Transmitter Release

Effects of cadmium on quantal transmitter release and ultrastructure of frog motor nerve endings

1989 ◽  
Vol 77 (2-3) ◽  
pp. 79-91 ◽  
Author(s):  
J. Molg� ◽  
M. P�cot-Dechavassine ◽  
S. Thesleff
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Quantal Transmitter Release

Inhibition of β-bungarotoxin action by bee venom phospholipase A 2

1978 ◽  
Vol 200 (1139) ◽  
pp. 225-230 ◽  
Keyword(s):  
Transmitter Release ◽  
Motor Nerve ◽  
Frog Muscle ◽  
Phospholipase A ◽  
Bee Venom ◽  
Nerve Endings ◽  
Low Concentration ◽  
External Fluid ◽  
Nerve Muscle ◽  
Endplate Potentials

β-Bungarotoxin (β-BuTX) induces twitching of innervated frog muscle and subsequently blocks transmitter release from motor nerve endings. These actions of β-BuTX are prevented if the nerve-muscle junctions are pretreated with a low concentration of phospholipase A 2 from bee venom. When the Ca 2+ in the external fluid is replaced by Sr 2+ , the phospho­lipase activity of β-BuTX is negligible and, in these conditions, β-BuTX causes a decrease in the amplitude of endplate potentials but does not go on to block transmitter release completely.

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