Evidence map›Paper›PMID 19940186›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Dopamine-stimulated dephosphorylation of connexin 36 mediates AII amacrine cell uncoupling.

W Wade Kothmann, Stephen C Massey, John O'Brien

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

121 citing papers in PubMed, 200 citations in OpenAlex.

  1. Defining the electrical synapse.Nature reviews. Neuroscience · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Trafficking of Connexin36 (Cx36) in the early secretory pathway.bioRxiv : the preprint server for biology · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. The Role of Retinal Dysfunction in Myopia Development.Cellular and molecular neurobiology · 2023
    Review

61 more citing papers are in PubMed but not listed here.

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.

W Wade KothmannRichard S. Ruiz Department of Ophthalmology, University of Texas Medical School at Houston, Houston, Texas 77030, USA. Wade.Kothmann@gmail.com
Stephen C Massey
John O'Brien
The University of Texas at Austin · US

Funding

REGULATION OF RETINAL GAP JUNCTIONSR01EY012857 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI JOHN O'BRIEN · 2000 to 2026
$8.3M
VISION RESEARCHP30EY010608 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MASSEY, STEPHEN C · 1994 to 2014
$7.9M
NEUROTRANSMITTER MECHANISMS IN THE RETINAR01EY006515 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MASSEY, STEPHEN C · 1985 to 2017
$7.0M
Regulation of connexin35/36-mediated coupling by phosphorylationF31NS063534 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOTHMANN, WILLIAM WADE · 2008 to 2009
$42k
NEUROTRANSMITTER MECHANISMS IN THE RETINAR55EY006515 · NEI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MASSEY, STEPHEN C. · 1991 to 1991
–
NEI NIH HHS EY06515NEI NIH HHS EY10608NEI NIH HHS EY12857NEI NIH HHS P30 EY010608NEI NIH HHS R01 EY006515NEI NIH HHS R01 EY012857NINDS NIH HHS F31 NS063534NINDS NIH HHS NS63534
6 · The paper itself

Abstract

Gap junction proteins form the substrate for electrical coupling between neurons. These electrical synapses are widespread in the CNS and serve a variety of important functions. In the retina, connexin 36 (Cx36) gap junctions couple AII amacrine cells and are a requisite component of the high-sensitivity rod photoreceptor pathway. AII amacrine cell coupling strength is dynamically regulated by background light intensity, and uncoupling is thought to be mediated by dopamine signaling via D(1)-like receptors. One proposed mechanism for this uncoupling involves dopamine-stimulated phosphorylation of Cx36 at regulatory sites, mediated by protein kinase A. Here we provide evidence against this hypothesis and demonstrate a direct relationship between Cx36 phosphorylation and AII amacrine cell coupling strength. Dopamine receptor-driven uncoupling of the AII network results from protein kinase A activation of protein phosphatase 2A and subsequent dephosphorylation of Cx36. Protein phosphatase 1 activity negatively regulates this pathway. We also find that Cx36 gap junctions can exist in widely different phosphorylation states within a single neuron, implying that coupling is controlled at the level of individual gap junctions by locally assembled signaling complexes. This kind of synapse-by-synapse plasticity allows for precise control of neuronal coupling, as well as cell-type-specific responses dependent on the identity of the signaling complexes assembled.

Indexed as

Amacrine CellsAnimalsCell CommunicationConnexinsCyclic AMP-Dependent Protein KinasesDopamineEnzyme ActivationGap Junction delta-2 ProteinGap JunctionsOrgan Culture TechniquesPhosphorylationProtein Phosphatase 1Protein Phosphatase 2RabbitsRetinaSignal TransductionConnexinsCyclic AMP-Dependent Protein KinasesDopamineGap Junction delta-2 ProteinProtein Phosphatase 1Protein Phosphatase 2

Identifiers

PMID19940186
PMCPMC2839935
OpenAlexW2075212294

What OpenQuestion holds

Textmetadata
LicenceTDM
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.