Influence of presynaptic receptors on neuromuscular transmission in rat

1982 ◽  
Vol 242 (5) ◽  
pp. C366-C372 ◽  
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.

scholarly journals The Frog Motor Nerve Terminal Has Very Brief Action Potentials and Three Electrical Regions Predicted to Differentially Control Transmitter Release

2020 ◽  
Vol 40 (18) ◽  
pp. 3504-3516 ◽  
Author(s):  
Scott P. Ginebaugh ◽  
Eric D. Cyphers ◽  
Viswanath Lanka ◽  
Gloria Ortiz ◽  
Evan W. Miller ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Transmitter Release ◽  
Action Potentials ◽  
Motor Nerve ◽  
Motor Nerve Terminal

The action of sodium pump inhibitors on neuromuscular transmission

1968 ◽  
Vol 170 (1021) ◽  
pp. 381-399 ◽  
Keyword(s):  
Action Potentials ◽  
Neuromuscular Transmission ◽  
Sodium Pump ◽  
Motor Nerve ◽  
Conduction Block ◽  
Progressive Increase ◽  
Frog Skeletal Muscle ◽  
End Plate ◽  
Quantum Content ◽  
Potential Frequency

Exposure of isolated frog skeletal muscle to a cardiac glycoside produces changes in the prejunctional events associated with neuromuscular transmission. The principal changes consist of a progressive increase in the quantum content of the end-plate potential, followed by conduction block in intramuscular motor nerve branches. These events are accompanied by a progressive increase in the frequency of miniature end-plate potentials. Following conduction blockade spontaneous end-plate potentials occur which arise from the generation of action potentials at or near the nerve terminations. Still later, the miniature end-plate potential frequency declines and the nerve endings become entirely inexcitable. These changes appear to result from inhibition of a sodium pump in the motor nerve axons and their endings.

The release of acetylcholine from nerve endings by graded electric pulses

1967 ◽  
Vol 167 (1006) ◽  
pp. 23-38 ◽  
Keyword(s):  
Nerve Ending ◽  
Transmitter Release ◽  
Motor Nerve ◽  
Motor Nerve Ending ◽  
Axon Membrane ◽  
Electric Pulses ◽  
End Plate ◽  
Calcium Compound ◽  
Release Of Acetylcholine ◽  
Positively Charged

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.

Different VAMP/Synaptobrevin Complexes for Spontaneous and Evoked Transmitter Release at the Crayfish Neuromuscular Junction

1998 ◽  
Vol 80 (6) ◽  
pp. 3233-3246 ◽  
Author(s):  
Shao-Ying Hua ◽  
Dorota A. Raciborska ◽  
William S. Trimble ◽  
Milton P. Charlton
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Neuromuscular Junctions ◽  
Spontaneous Release ◽  
Intracellular Ca ◽  
Crayfish Neuromuscular Junction ◽  
Evoked Transmitter Release

Hua, Shao-Ying, Dorota A. Raciborska, William S. Trimble, and Milton P. Charlton. Different VAMP/synaptobrevin complexes for spontaneous and evoked transmitter release at the crayfish neuromuscular junction. J. Neurophysiol. 80: 3233–3246, 1998. Although vesicle-associated membrane protein (VAMP/synaptobrevin) is essential for evoked neurotransmitter release, its role in spontaneous transmitter release remains uncertain. For instance, many studies show that tetanus toxin (TeNT), which cleaves VAMP, blocks evoked transmitter release but leaves some spontaneous transmitter release. We used recombinant tetanus and botulinum neurotoxin catalytic light chains (TeNT-LC, BoNT/B-LC, and BoNT/D-LC) to examine the role of VAMP in spontaneous transmitter release at neuromuscular junctions (nmj) of crayfish. Injection of TeNT-LC into presynaptic axons removed most of the VAMP immunoreactivity and blocked evoked transmitter release without affecting nerve action potentials or Ca2+ influx. The frequency of spontaneous transmitter release was little affected by the TeNT-LC when the evoked transmitter release had been blocked by >95%. The spontaneous transmitter release left after TeNT-LC treatment was insensitive to increases in intracellular Ca2+. BoNT/B-LC, which cleaves VAMP at the same site as TeNT-LC but uses a different binding site, also blocked evoked release but had minimal effect on spontaneous release. However, BoNT/D-LC, which cleaves VAMP at a different site from the other two toxins but binds to the same position on VAMP as TeNT, blocked both evoked and spontaneous transmitter release at similar rates. The data indicate that different VAMP complexes are employed for evoked and spontaneous transmitter release; the VAMP used in spontaneous release is not readily cleaved by TeNT or BoNT/B. Because the exocytosis that occurs after the action of TeNT cannot be increased by increased intracellular Ca2+, the final steps in neurotransmitter release are Ca2+ independent.

scholarly journals Acute Functional Adaptations in Isolated Presynaptic Terminals Unveil Synaptosomal Learning and Memory

2019 ◽  
Vol 20 (15) ◽  
pp. 3641 ◽  
Author(s):  
Anna Pittaluga
Keyword(s):  
Transmitter Release ◽  
Presynaptic Receptors ◽  
Chemical Stimulation ◽  
Functional Adaptation ◽  
Pathological Conditions ◽  
Chemical Agents ◽  
Important Progress

Synaptosomes are used to decipher the mechanisms involved in chemical transmission, since they permit highlighting the mechanisms of transmitter release and confirming whether the activation of presynaptic receptors/enzymes can modulate this event. In the last two decades, important progress in the field came from the observations that synaptosomes retain changes elicited by both “in vivo” and “in vitro” acute chemical stimulation. The novelty of these studies is the finding that these adaptations persist beyond the washout of the triggering drug, emerging subsequently as functional modifications of synaptosomal performances, including release efficiency. These findings support the conclusion that synaptosomes are plastic entities that respond dynamically to ambient stimulation, but also that they “learn and memorize” the functional adaptation triggered by acute exposure to chemical agents. This work aims at reviewing the results so far available concerning this form of synaptosomal learning, also highlighting the role of these acute chemical adaptations in pathological conditions.

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