ArticlePflugers Archiv : European journal of physiology1991
Evoked phasic release in frog nerve terminals obtained after block of Ca2+ entry by Cd2+.
Article in Pflugers Archiv : European journal of physiology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Bayesian analysis of the kinetics of quantal transmitter secretion at the neuromuscular junction.Journal of computational neuroscience · 2015Article
- Determining Ca2+-sensor binding time and its variability in evoked neurotransmitter release.The Journal of physiology · 2008Article
- Contribution of Ca2+ inflow to quantal, phasic transmitter release from nerve terminals of frog muscle.Pflugers Archiv : European journal of physiology · 1992Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous pectoris muscles of frogs were isolated, mounted in a chamber and superfused with Ringer's solution. With a macro-patch-clamp electrode placed on a section of a motor nerve terminal, quantal synaptic currents were elicited by depolarizing pulses and recorded. The electrode tip and the section of the terminal recorded from were perfused rapidly by Ringer's solution alone or containing 20-500 microM Cd2+ to block Ca2+ inflow. Separate superfusion of the muscle and the rest of the terminal with normal or elevated Ca2+ Ringer's solution provided a sufficiently high resting Ca2+ concentration in the terminal even when Ca2+ was blocked by Cd2+. The depolarization level of maximal Ca2+ inflow into the terminal was found by measuring maximal test pulse facilitation, Fc. In control solution as well as in the case of Cd2+ block, the rate of phasic release after depolarizing pulses rose further when depolarization was increased past the level of Fc, and reached a saturation level which was maintained at estimated depolarizations up to +200 mV. Block of Ca2+ inflow by Cd2+ decreased release substantially, but did not suppress it. The depression of release was greater in the range of large Ca2+ inflow (around Fc) than for very large depolarizations. The time course of phasic release was unaltered by blockage of Ca2+ inflow. It is concluded that Ca2+ inflow contributes to the promotion of evoked release only in the depolarization range in which Ca2+ inward current is large.(ABSTRACT TRUNCATED AT 250 WORDS)
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.