ATP and adenosine inhibit transmitter release at the frog neuromuscular junction through distinct presynaptic receptors

@article{Giniatullin1998ATPAA,
  title={ATP and adenosine inhibit transmitter release at the frog neuromuscular junction through distinct presynaptic receptors},
  author={R. A. Giniatullin and Elena Sokolova},
  journal={British Journal of Pharmacology},
  year={1998},
  volume={124}
}
The effects of exogenous ATP or adenosine on end‐plate currents (e.p.cs; evoked by simultaneous action of a few hundred quanta of ACh) or on miniature e.p.cs (m.e.p.cs) were studied under voltage clamp conditions on frog sartorius muscle fibres. ATP or adenosine (100 μM–1 mM) reduced the e.p.c. amplitude but did not affect m.e.p.c. amplitude, decay time constant and voltage‐dependence of m.e.p.c., suggesting that e.p.c. depression induced by these purines had presynaptic origin only. The action… Expand
Distinct receptors and different transduction mechanisms for ATP and adenosine at the frog motor nerve endings
TLDR
The authors' data indicate, for motor nerve endings, the existence of inhibitory P2Y receptors coupled to multiple intracellular cascades including phosphatidylinositide‐specific PLC/PKC/PLA2/COX, which could provide feedback inhibition of transmitter release and perhaps be involved in presynaptic plasticity. Expand
Mechanisms of ATP action on motor nerve terminals at the frog neuromuscular junction
TLDR
The presynaptic depressant action of ATP is mediated by inhibition ofCa2+ channels and by mechanism acting downstream of Ca2+ entry, suggesting Ca2‐dependence of the ATP action. Expand
Presynaptic inhibition of spontaneous acetylcholine release mediated by P2Y receptors at the mouse neuromuscular junction
TLDR
Results show that at mammalian neuromuscular junctions, ATP induces presynaptic inhibition of spontaneous ACh release due to the modulation of Ca(2+) channels related to tonic secretion through the activation of P2Y receptors coupled to G(i/o) proteins. Expand
P2Y13 receptors mediate presynaptic inhibition of acetylcholine release induced by adenine nucleotides at the mouse neuromuscular junction
TLDR
It is concluded that, at motor nerve terminals, the Gi/o protein-coupled P2y receptors implicated in presynaptic inhibition of spontaneous and evoked ACh release are of the subtype P2Y13, which provides new insights into the types of purinergic receptors that contribute to the fine-tuning of cholinergic transmission at mammalian neuromuscular junction. Expand
ATP but not adenosine inhibits nonquantal acetylcholine release at the mouse neuromuscular junction
TLDR
The postsynaptic membrane of the neuromuscular synapse treated with antiacetylcholinesterase is depolarized due to nonquantal release of acetylcholine (ACh) from the motor nerve ending, and hyperpolarization produced by the application of curare (H‐effect) shows that nonquantAL release of ACh can be modulated by several distinct regulatory pathways. Expand
Modulatory Role of Adenosine Receptors in Insect Motor Nerve Terminals
TLDR
The results show for the first time the presence of presynapticAdenosine receptors regulating transmitter release at insect motor nerve terminals and point to differences in pharmacological properties of adenosine receptor subtypes in insects and vertebrates. Expand
Purine P2Y receptors in ATP-mediated regulation of non-quantal acetylcholine release from motor nerve endings of rat diaphragm
TLDR
ATP regulates the neuromuscular synapse by two different pathways via P2Y receptors coupled to G(q/11) and PLC, and can be explained by the independence of the action of ATP and glutamate. Expand
Endogenous purines modulate K+‐evoked ACh secretion at the mouse neuromuscular junction
TLDR
When motor nerve terminals are depolarized by increasing K+ concentrations, the ATP/ADP and adenosine endogenously generated are able to modulate ACh secretion by sequential activation of different purinergic receptors. Expand
Adenosine Promotes Endplate nAChR Channel Activity in Adult Mouse Skeletal Muscle Fibers via Low Affinity P1 Receptors
TLDR
The data suggest that at the adult mammalian NMJ, adenosine acts not only presynaptically to modulate acetylcholine transmitter release, but also at the postsynaptic level, to enhance the activity of nAChRs at the mammalian endplate region. Expand
ATP is released from nerve terminals and from activated muscle fibres on stimulation of the rat phrenic nerve
TLDR
The presently observed post- Synaptic release of ATP together with the previously reported lack of post-synaptic effects of ATP and to the ability of ATP to act as a presynaptic modulator open the possibility that ATP may behave as a retrograde messenger at this neuromuscular junction. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 28 REFERENCES
Autoreceptor‐mediated purinergic and cholinergic inhibition of motor nerve terminal calcium currents in the rat.
TLDR
The results indicate that ATP and ACh, which are released during exocytosis, may inhibit their own release through attenuation of the terminal Ca2+ current via autoreceptors coupled to a G protein. Expand
THE EFFECTS OF ADENOSINE TRIPHOSPHATE AND ADENOSINE DIPHOSPHATE ON TRANSMISSION AT THE RAT AND FROG NEUROMUSCULAR JUNCTIONS
TLDR
The potency of ATP was found to be similar to that of adenosine, and the addition of ATP had no further effect, compatible with the idea that ATP acts in the same way asadenosine. Expand
Purinergic regulation of acetylcholine release.
TLDR
To find out precisely what occurs with ACh in transmitting its message at the synaptic level, one has to consider the subtle ways used by purines to modulate the ACh response. Expand
Chapter 23 Purinergic regulation of acetylcholine release
Publisher Summary At the neuromuscular junction and possibly also at the synaptic level in the brain, the main sequence of events that involves purines in modulation of acetylcholine (ACh) releaseExpand
Synchronous release of ATP and neurotransmitter within milliseconds of a motor nerve impulse in the frog.
TLDR
The results suggest that ATP is released synchronously together with the neurotransmitter ACh in response to an individual nerve impulse and with a brief latency characteristic of quantal release from synaptic vesicles. Expand
Endogenous adenosine modulates stimulation‐induced depression at the frog neuromuscular junction.
TLDR
When nerve terminals are pooled according to their individual release characteristics, endogenous adenosine can be shown to contribute significantly to stimulation‐induced depression of release primarily in terminals that release enough transmitter to generate significant levels ofAdenosine, but do not release so much transmitter that depletion of releasable quanta is severe. Expand
ATP released together with acetylcholine as the mediator of neuromuscular depression at frog motor nerve endings.
TLDR
In conclusion, endogenous ATP, after hydrolysis to adenosine, causes prejunctional neuromuscular depression in this species and is confirmed by earlier findings that ATP must be hydrolysed toAdenosine to inhibit ACh release. Expand
Sources of adenosine released during neuromuscular transmission in the rat.
  • D. O. Smith
  • Biology, Medicine
  • The Journal of physiology
  • 1991
TLDR
It is concluded that adenine nucleotides (presumably in the form of ATP) and ACh are released jointly, and that ATP is hydrolysed fairly rapidly to adenosine. Expand
Purinergic receptors and their activation by endogenous purines at perisynaptic glial cells of the frog neuromuscular junction
  • R. Robitaille
  • Biology, Medicine
  • The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1995
TLDR
It is shown that blockade of ATP receptors reduced the size and increased the delay of the responses of glial Ca2+ responses, Hence, purinoceptors are present on the perisynaptic Schwann cells and are activated by endogenous ATP released during synaptic transmission. Expand
An ATP-activated, ligand-gated ion channel on a cholinergic presynaptic nerve terminal.
  • X. P. Sun, E. F. Stanley
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1996
TLDR
ATP was pulsed onto the terminals under voltage clamp and induced a short latency cation current that exhibited inward rectification and marked desensitization, and a ligand-gated P2X-like purinergic receptor on a cholinergic presynaptic nerve terminal was demonstrated. Expand
...
1
2
3
...