Evidence map›Paper›PMID 19403749›Full record

ArticleJournal of neurophysiology2009

Extrasynaptic release of GABA by retinal dopaminergic neurons.

Hajime Hirasawa, Michelino Puopolo, Elio Raviola

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

23 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Do you have restless leg syndrome? I understood from your eyes.Sleep & breathing = Schlaf & Atmung · 2019
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Serotonin release from the neuronal cell body and its long-lasting effects on the nervous system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  13. Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Corelease of dopamine and GABA by a retinal dopaminergic neuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  19. Article
  20. The tasks of amacrine cells.Visual neuroscience · 2012
    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

3 authors at 1 institution in 1 country.

Hajime HirasawaDepartment of Neurobiology, Harvard Medical School, 220 Longwood Ave., Boston, MA 02115, USA.
Michelino Puopolo
Elio Raviola
Harvard University · US

Funding

CELL BIOLOGY OF THE RETINAR01EY001344 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI RAVIOLA, ELIO S · 1985 to 2009
$6.3M
NEI NIH HHS EY-01344
6 · The paper itself

Abstract

GABA release by dopaminergic amacrine (DA) cells of the mouse retina was detected by measuring Cl- currents generated by isolated perikarya in response to their own neurotransmitter. The possibility that the Cl- currents were caused by GABA release from synaptic endings that had survived the dissociation of the retina was ruled out by examining confocal Z series of the surface of dissociated tyrosine hydroxylase-positive perikarya after staining with antibodies to pre and postsynaptic markers. GABA release was caused by exocytosis because 1) the current events were transient on the millisecond time scale and thus resembled miniature synaptic currents; 2) they were abolished by treatment with a blocker of the vesicular proton pump, bafilomycin A1; and 3) their frequency was controlled by the intracellular Ca2+ concentration. Because DA cell perikarya do not contain presynaptic active zones, release was by necessity extrasynaptic. A range of depolarizing stimuli caused GABA exocytosis, showing that extrasynaptic release of GABA is controlled by DA cell electrical activity. With all modalities of stimulation, including long-lasting square pulses, segments of pacemaker activity delivered by the action-potential-clamp method and high-frequency trains of ramps, discharge of GABAergic currents exhibited considerable variability in latency and duration, suggesting that coupling between Ca2+ influx and transmitter exocytosis is extremely loose in comparison with the synapse. Paracrine signaling based on extrasynaptic release of GABA by DA cells and other GABAergic amacrines may participate in controlling the excitability of the neuronal processes that interact synaptically in the inner plexiform layer.

Indexed as

AnimalsCadmiumCalciumCells, CulturedCesiumChloridesDopamineDose-Response Relationship, DrugElectric StimulationEnzyme InhibitorsExocytosisGABA Antagonistsgamma-Aminobutyric AcidMacrolidesMembrane PotentialsMicebafilomycin A1CadmiumCalciumCesiumcesium chlorideChloridesDopamineEnzyme InhibitorsGABA Antagonistsgabazinegamma-Aminobutyric AcidMacrolidesPyridazinesSodium Channel BlockersSynapsinsTetrodotoxinTyrosine 3-Monooxygenase

Identifiers

PMID19403749
PMCPMC2712262
OpenAlexW1000466968

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.