Evidence map›Paper›PMID 18667624›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Diverse mechanisms underlie glycinergic feedback transmission onto rod bipolar cells in rat retina.

Andrés E Chávez, Jeffrey S Diamond

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Article
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  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Rod-cone crossover connectome of mammalian bipolar cells.The Journal of comparative neurology · 2019
    Article
  10. Article
  11. Article
  12. Low concentrations of ethanol but not of dimethyl sulfoxide (DMSO) impair reciprocal retinal signal transduction.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Nonsynaptic NMDA receptors mediate activity-dependent plasticity of gap junctional coupling in the AII amacrine cell network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  20. Receptor targets 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

2 authors.

Andrés E ChávezSynaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3701, USA. achavez@aecom.yu.edu
Jeffrey S Diamond

Funding

Synaptic Mechanisms in the Mammalian RetinaZIANS003039 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI DIAMOND, JEFFREY S · 2009 to 2025
$24.5M
Synaptic Mechanisms in the Mammalian RetinaZ01NS003039 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI DIAMOND, JEFFREY S · 2007 to 2008
$2.8M
Intramural NIH HHS Z01 NS003039
6 · The paper itself

Abstract

Synaptic inhibition shapes visual signaling in the inner retina, but the physiology of most amacrine cells, the interneurons that mediate this inhibition, is poorly understood. Discerning the function of most individual amacrine cell types is a daunting task, because few molecular or morphological markers specifically distinguish between approximately two dozen different amacrine cell types. Here, we examine a functional subset of amacrine cells by pharmacologically isolating glycinergic inhibition and evoking feedback IPSCs in a single cell type, the rod bipolar cell (RBC), with brief glutamate applications in the inner plexiform layer. We find that glycinergic amacrine cells innervating RBCs receive excitatory inputs from ON and OFF bipolar cells primarily via NMDA receptors (NMDARs) and Ca2+-impermeable AMPA-type glutamate receptors. Glycine release from amacrine cells is triggered by Ca2+ influx through both voltage-gated Ca2+ (Ca(v)) channels and NMDARs. These intracellular Ca2+signals are amplified by Ca2+-induced Ca2+ release via both ryanodine and IP3 receptors, which are activated independently by Ca2+ influx through Ca(v) channels and NMDARs, respectively. Glycinergic feedback signaling depends strongly, although not completely, on voltage-gated Na+ channels, and the spatial extent of feedback inhibition is expanded by gap junction connections between glycinergic amacrine cells. These results indicate that a diversity of mechanisms underlie glycinergic feedback inhibition onto RBCs, yet they highlight several physiological themes that appear to distinguish amacrine cell function.

Indexed as

AnimalsFeedback, PhysiologicalGlycineMiceMice, Inbred C57BLRatsRats, Sprague-DawleyRetinaRetinal Bipolar CellsRetinal Rod Photoreceptor CellsSynaptic TransmissionGlycine

Identifiers

PMID18667624
PMCPMC2575372

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.