Evidence map›Paper›PMID 12640015›Full record

ArticleThe Journal of physiology2003

Intraterminal Ca2+ concentration and asynchronous transmitter release at single GABAergic boutons in rat collicular cultures.

Sergei Kirischuk, Rosemarie Grantyn

Abstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. The Parvalbumin Hypothesis of Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2020
    Article
  3. Article
  4. Review
  5. Article
  6. An alien divalent ion reveals a major role for Ca²⁺ buffering in controlling slow transmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Adaptation reduces spike-count reliability, but not spike-timing precision, of auditory nerve responses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  16. Ambient GABA constrains the strength of GABAergic synapses at Cajal-Retzius cells in the developing visual cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  17. Article
  18. Article
  19. Developmental changes in parvalbumin regulate presynaptic Ca2+ signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
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

2 authors.

Sergei KirischukDevelopmental Physiology, Johannes Müller Institute of Physiology, Humboldt University Medical School (Charité), 10117 Berlin, Germany. sergei.kirischuk@charite.de
Rosemarie Grantyn

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotransmitter release in response to a single action potential has a precise time course. A significant fraction of the releasable vesicles is exocytosed synchronously, within a few milliseconds after the arrival of an action potential. If repeatedly activated, stimulus-locked phasic synchronous release declines, but synaptic transmission can be maintained through tonic asynchronous transmitter release. The desynchronisation of release during repetitive activation is generally attributed to a build-up of intraterminal Ca2+ concentration. However, the precise relationship between presynaptic Ca2+ level and asynchronous release rate at small central synapses has remained unclear. Here we characterise this relationship for single GABAergic terminals in rat collicular cultures. In the presence of tetrodotoxin, inhibitory postsynaptic currents (IPSCs) and presynaptic Ca2+ transients were recorded in response to direct presynaptic depolarisation of individual boutons. Repetitive stimulation indeed resulted in a shift from phasic to asynchronous neurotransmitter release. A clear dominance of the asynchronous release mode was observed after 10 pulses. The steady-state asynchronous release rate showed a third-power dependency on the presynaptic Ca2+ concentration, which is similar to that of evoked release. The Ca2+ sensor for asynchronous release exhibited a high affinity for Ca2+ and was far from saturation. These properties of the Ca2+ sensor should make the asynchronous release very sensitive to any modification of presynaptic Ca2+ concentration, including those resulting from changes in presynaptic activity patterns. Thus, asynchronous release represents a powerful but delicately regulated mechanism that ensures the maintenance of appropriate inhibition when the readily releasable pool of vesicles is depleted.

Indexed as

AnimalsAnimals, NewbornCalciumCells, CulturedElectric StimulationEvoked PotentialsExcitatory Postsynaptic Potentialsgamma-Aminobutyric AcidKineticsNeuronsNeurotransmitter AgentsPatch-Clamp TechniquesRatsSuperior ColliculiTime FactorsCalciumgamma-Aminobutyric AcidNeurotransmitter Agents

Identifiers

PMID12640015
PMCPMC2342888

What OpenQuestion holds

Textmetadata
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.