Evidence map›Paper›PMID 10087345›Full record

ArticleThe Journal of physiology1999

Two components of transmitter release from the chick ciliary presynaptic terminal and their regulation by protein kinase C.

H Yawo

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 31% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Phosphorylation-dependent low-frequency depression at phasic synapses of a crayfish motoneuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  4. Increase in the pool size of releasable synaptic vesicles by the activation of protein kinase C in goldfish retinal bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  5. Probing fundamental aspects of synaptic transmission with strontium.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  6. Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

H YawoNeurophysiology Division, Department of Physiology and Pharmacology, Tohoku University School of Medicine, Sendai 980-8575, Japan. yawo@mail.cc.tohoku.ac.jp
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. A study was made of the effects of phorbol ester (phorbol 12-myristate 13-acetate, PMA, 0.1 microM) on the two components of evoked transmitter release, namely the fast synchronous and the slow asynchronous components, from the giant presynaptic terminal of the chick ciliary ganglion. The excitatory postsynaptic currents (EPSCs) were recorded under whole-cell voltage clamp of the postsynaptic neuron. 2. The decay time constant of the slow component was prolonged by replacing Ca2+ with Sr2+. In 5 mM [Sr2+]o the fast component decayed with a time constant of 2.6 +/- 1.4 ms whereas the slow component decayed with a time constant of 19 +/- 7 ms. 3. When stimulated with twin pulses with a short interpulse interval, the fast component of the second EPSC was often depressed whereas the slow component was usually facilitated. Both components were positively dependent on [Sr2+]o in a saturable manner, but the fast component approached its maximum at a lower [Sr2+]o than the slow component. 4. PMA potentiated both the fast and slow components to a similar extent and with a similar time course. For each component, the effect of PMA was less potent at high [Sr2+]o than at low [Sr2+]o. For either the fast or the slow component the PMA-induced potentiation was accompanied by a reduction in the paired-pulse ratio (PPR). 5. Despite the different dissociation constant for dextran-conjugated fura-2, the fluorescent ratio for intraterminal [Sr2+] ([Sr2+]i) decayed to the baseline after the nerve-evoked increment with a time course similar to that for [Ca2+]i, suggesting that intraterminal Sr2+ is buffered less efficiently than Ca2+. PMA did not increase the [Sr2+]i transients produced by stimulation of the presynaptic oculomotor nerve. 6. It is suggested that protein kinase C (PKC) modulates both the fast and slow components through common molecular mechanisms that upregulate the Sr2+ sensitivity of the vesicle fusion probability.

Indexed as

AlgorithmsAnimalsCalciumChick EmbryoElectric StimulationExcitatory Postsynaptic PotentialsFluorescent DyesFura-2Ganglia, ParasympatheticNeurotransmitter AgentsProtein Kinase CReceptors, PresynapticStrontiumTetradecanoylphorbol AcetateUp-RegulationCalciumFluorescent DyesFura-2Neurotransmitter AgentsProtein Kinase CReceptors, PresynapticStrontiumTetradecanoylphorbol Acetate

Identifiers

PMID10087345
PMCPMC2269278
OpenAlexW2091279432

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

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.