Temperature Effect on Carbachol-Induced Depression of Spontaneous Quantal Transmitter Release in Frog Neuromuscular Junction

@article{Strunsky2001TemperatureEO,
  title={Temperature Effect on Carbachol-Induced Depression of Spontaneous Quantal Transmitter Release in Frog Neuromuscular Junction},
  author={E. G. Strunsky and Mikhail Borisover and E. E. Nikolsky and Frantisek Vyskocil},
  journal={Neurochemical Research},
  year={2001},
  volume={26},
  pages={891-897}
}
The effects of carbachol (CCh) on the frequency (f) of the miniature endplate potentials were tested at temperatures between 5 and 30°C. Higher CCh concentrations, 1 × 10−5 and 5 × 10−6 M, reduced the f to 60% and the temperature dependence was negligible. However, an inverse temperature dependence was found when low concentrations 3 × 10−7 and 6 × 10−7 M were applied. The depression of f was 40–50% in 5–10°C but only 10–20% of the control in the 25 and 30°C. During application of CCh, the new… 

Temperature Effect on Proximal to Distal Gradient of Quantal Release of Acetylcholine at Frog Endplate

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.

Negative cross‐talk between presynaptic adenosine and acetylcholine receptors

It is proposed that the negative cross‐talk between two major autoreceptors could take place during intense synaptic activity and thereby attenuate the presynaptic inhibitory effects of ACh and adenosine.

References

SHOWING 1-10 OF 26 REFERENCES

Depression of miniature endplate potential frequency by acetylcholine and its analogues in frog

Low temperature‐dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics, in contrast to previous reports.

The effect of temperature on desensitization kinetics at the post‐synaptic membrane of the frog muscle fibre.

The rate of onset and the rate of recovery changed with temperature in the case of intracellular potentiation of desensitization, in a similar manner to that observed after extracellular application of these drugs.

Noise analysis of drug induced voltage clamp currents in denervated frog muscle fibres.

The autocorrelation function of drug‐induced current fluctuations, recorded at the former end‐plate region of chronically denervated fibres often shows both a fast and a slow time constant, which could indicate that two populations of channels exist at theFormer end‐ plate region ofDenervated muscle fibres.

Inhibitory effects of cholinergic agents on the release of transmitter at the frog neuromuscular junction.

It is concluded that non‐specific cholinesterases present on the presynaptic terminals can act as inhibitory muscarinic cholinergic receptors at the amphibian neuromuscular junction and that the consequent reduction in Ca2+ entry causes a fall in both evoked release and in intracellular Ca2+.

Stimulation‐induced factors which affect augmentation and potentiation of trasmitter release at the neuromuscular junction.

The magnitude of augmentation following the secondary conditioning trains was increased over that following the primary conditioning trains even though augmentation, with a time constant of decay of about 7 sec, had decayed to insignificant levels before the onset of the secondary trains.

The effect of temperature on the sodium and potassium permeability changes in myelinated nerve fibres of Xenopus laevis

The purpose of the present investigation was to determine the effects which changes in temperature have on the constants governing the permeability changes in the myelinated nerve fibre. Voltage

Kinetics, Ca2+ Dependence, and Biophysical Properties of Integrin-Mediated Mechanical Modulation of Transmitter Release from Frog Motor Nerve Terminals

It is postulated that tension on integrins in the presynaptic membrane is transduced mechanically into changes in the position or conformation of one or more molecules involved in neurotransmitter release, altering sensitivity to Ca2+ or the equilibrium for a critical reaction leading to vesicle fusion.