Cholinergic regulation of the evoked quantal release at frog neuromuscular junction

@article{Nikolsky2004CholinergicRO,
  title={Cholinergic regulation of the evoked quantal release at frog neuromuscular junction},
  author={Eugen E. Nikolsky and Frantisek Vyskocil and E. A. Bukharaeva and Dmitry V. Samigullin and Lev G Magazanik},
  journal={The Journal of Physiology},
  year={2004},
  volume={560}
}
The effects of cholinergic drugs on the quantal contents of the nerve‐evoked endplate currents (EPCs) and the parameters of the time course of quantal release (minimal synaptic latency, main modal value of latency histogram and variability of synaptic latencies) were studied at proximal, central and distal regions of the frog neuromuscular synapse. Acetylcholine (ACh, 5 × 10−4m), carbachol (CCh, 1 × 10−5m) or nicotine (5 × 10−6m) increased the numbers of EPCs with long release latencies mainly… Expand
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References

SHOWING 1-10 OF 72 REFERENCES
Noradrenaline synchronizes evoked quantal release at frog neuromuscular junctions
TLDR
The synchronizing action of NA might potentiate neuromuscular transmission during nerve regeneration, transmitter exhaustion and other extreme physiological states where the quantal content is reduced, such as survival in cold and hibernation. Expand
Muscarinic modulation of neurotransmission: the effects of some agonists and antagonists.
TLDR
A more complicated pattern related to the muscarinic action at the mouse neuromuscular junction with the involvement of some post-synaptic located sites is suggested. Expand
Presynaptic M2 muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction
1 Macropatch recording was used to study release of acetylcholine in the frog neuromuscular junction evoked by either direct local depolarization or by an action potential. 2 The quantal content wasExpand
Characteristics of the Time Course of Evoked Secretion of Transmitter Quanta in Different Parts of the Motor Nerve Ending in the Frog
Experiments were performed on neuromuscular preparations from frogs, in which three extracellular microelectrodes were used to record nerve ending currents and single-quantum endplate currentsExpand
Modulation of ACh release by presynaptic muscarinic autoreceptors in the neuromuscular junction of the newborn and adult rat
TLDR
The way in which M1 and M2 muscarinic receptors modulate neurotransmission can differ between the developing and adult rat neuromuscular synapse is shown. Expand
Presynaptic effects of muscarine on ACh release at the frog neuromuscular junction
TLDR
Results show that the M2 receptor isresponsible for inhibition of ACh release, while the M1 receptor is responsible for its enhancement, and the inhibitory effect of muscarine did not depend on extracellular [Ca2+]. Expand
Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate
TLDR
The results show that protein kinase A is involved in the timing of quantal release and can be regulated by presynaptic adrenergic receptors. Expand
Temperature Effect on Proximal to Distal Gradient of Quantal Release of Acetylcholine at Frog Endplate
TLDR
The secretion synchronization, which is greatest in distal parts, compensates at least partly for the progressive slowing of spike conduction velocity in the proximodistal direction, in particular at lower temperatures. Expand
Long release latencies are increased by acetylcholine at frog endplate.
TLDR
P90, which is designated as the interval between the minimal synaptic delay and the time at which 90 per cent of all measured uni-quantal EPCs had occurred, was significantly and reversibly increased, indicating that the evoked release pattern is less synchronous and the increased asynchrony leads to a substantial drop in the amplitude of reconstructed multi-quantAL currents. Expand
Prejunctional modulation of acetylcholine release from the skeletal neuromuscular junction: link between positive (nicotinic)− and negative (muscarinic)‐feedback modulation
TLDR
It is concluded that quantally‐released ACh from motor endplates is subject to prejunctional automodulation: (a) ACh facilitates its own release via an effect on prejunctionsal nicotinic receptors (positive feedback), (b) A choline release is reduced by an action on muscarinic receptors. Expand
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