Evidence map›Paper›PMID 19332496›Full record

ArticleThe Journal of physiology2009

Switching between transient and sustained signalling at the rod bipolar-AII amacrine cell synapse of the mouse retina.

Josefin Snellman, David Zenisek, Scott Nawy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Multiple Calcium Channel Types with Unique Expression Patterns Mediate Retinal Signaling at Bipolar Cell Ribbon Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  8. Article
  9. Rapid and coordinated processing of global motion images by local clusters of retinal ganglion cells.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Paired-pulse plasticity in the strength and latency of light-evoked lateral inhibition to retinal bipolar cell terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  14. The mode of retinal presynaptic inhibition switches with light intensity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Trigger features and excitation in the retina.Current opinion in neurobiology · 2011
    Review
  20. 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

3 authors at 2 institutions in 1 country.

Josefin SnellmanYale University School of Medicine, Department of Cellular and Molecular Physiology, New Haven, CT 06520, USA.
David Zenisek
Scott Nawy
Yale University · USAlbert Einstein College of Medicine · US

Funding

Retinal Synaptic TransmissionR01EY014990 · NEI · YALE UNIVERSITY · PI ZENISEK, DAVID PAUL · 2003 to 2015
$5.2M
MECHANISMS OF SYNAPTIC TRANSMISSION IN THE RETINAR01EY010254 · NEI · YESHIVA UNIVERSITY · PI NAWY, SCOTT · 1993 to 2013
$4.2M
NEI NIH HHS EY010254NEI NIH HHS EY014990NEI NIH HHS R01 EY010254NEI NIH HHS R01 EY014990
6 · The paper itself

Abstract

At conventional synapses, invasion of an action potential into the presynaptic terminal produces a rapid Ca(2+) influx and ultimately the release of synaptic vesicles. However, retinal rod bipolar cells (RBCs) generally do not produce action potentials, and the rate of depolarization of the axon terminal is instead governed by the rate of rise of the light response, which can be quite slow. Using paired whole-cell recordings, we measured the behaviour of the RBC-AII amacrine cell synapse while simulating light-induced depolarizations either by slowly ramping the RBC voltage or by depolarizing the RBC with the mGluR6 receptor antagonist (R,S)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG). Both voltage ramps and CPPG evoked slow activation of presynaptic Ca(2+) currents and severely attenuated the early, transient component of the AII EPSC compared with voltage steps. We also found that the duration of the transient component was limited in time, and this limitation could not be explained by vesicle depletion, inhibitory feedback, or proton inhibition. Limiting the duration of the fast transient insures the availability of readily releasable vesicles to support a second, sustained component of release. The mGluR6 pathway modulator cGMP sped the rate of RBC depolarization in response to puffs of CPPG and consequently potentiated the transient component of the EPSC at the expense of the sustained component. We conclude that the rod bipolar cell is capable of both transient and sustained signalling, and modulation of the mGluR6 pathway by cGMP allows the RBC to switch between these two time courses of transmitter release.

Indexed as

Synaptic TransmissionVision, OcularAmacrine CellsAnimalsCalcium SignalingCyclic GMPExcitatory Postsynaptic PotentialsGlycineIn Vitro TechniquesKineticsMiceMice, Inbred C57BLPatch-Clamp TechniquesPresynaptic TerminalsReceptors, Metabotropic GlutamateRetinal Rod Photoreceptor CellsCyclic GMPcyclopropyl-4-phosphonophenylglycineGlycinemetabotropic glutamate receptor 6Receptors, Metabotropic Glutamate

Identifiers

PMID19332496
PMCPMC2714012
OpenAlexW1578511111

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.