Evidence map›Paper›PMID 16777935›Full record

ArticleThe Journal of physiology2006

Calcium channel and glutamate receptor activities regulate actin organization in salamander retinal neurons.

Massimiliano Cristofanilli, Abram Akopian

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 39% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  7. Fixation strategies for retinal immunohistochemistry.Progress in retinal and eye research · 2015
    Review
  8. Article
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  13. Review
  14. Glutamatergic signaling maintains the epithelial phenotype of proximal tubular cells.Journal of the American Society of Nephrology : JASN · 2011
    Article
  15. Article
  16. Article
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  19. Article
  20. Magnetic microposts as an approach to apply forces to living cells.Proceedings of the National Academy of Sciences of the United States of America · 2007
    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 at 1 institution in 1 country.

Massimiliano CristofanilliDepartment of Ophthalmology, New York University School of Medicine, 550 First Avenue PHL 843, New York, NY 10016, USA.
Abram Akopian
New York University · US

Funding

NEUROMODULATION OF RETINAL GANGLION CELL RESPONSESR01EY012497 · NEI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI AKOPIAN, ABRAM · 2000 to 2007
$2.2M
NEI NIH HHS EY 12497NEI NIH HHS R01 EY012497
6 · The paper itself

Abstract

Intracellular Ca2+ regulates a variety of neuronal functions, including neurotransmitter release, protein phosphorylation, gene expression and synaptic plasticity. In a variety of cell types, including neurons, Ca2+ is involved in actin reorganization, resulting in either actin polymerization or depolymerization. Very little, however, is known about the relationship between Ca2+ and the actin cytoskeleton organization in retinal neurons. We studied the effect of high-K+-induced depolarization on F-actin organization in salamander retina and found that Ca2+ influx through voltage-gated L-type channels causes F-actin disruption, as assessed by 53 +/- 5% (n = 23, P < 0.001) reduction in the intensity of staining with Alexa-Fluor488-phalloidin, a compound that permits visualization and quantification of polymerized actin. Calcium-induced F-actin depolymerization was attenuated in the presence of protein kinase C antagonists, chelerythrine or bis-indolylmaleimide hydrochloride (GF 109203X). In addition, phorbol 12-myristate 13-acetate (PMA), but not 4alpha-PMA, mimicked the effect of Ca2+ influx on F-actin. Activation of ionotropic AMPA and NMDA glutamate receptors also caused a reduction in F-actin. No effect on F-actin was exerted by caffeine or thapsigargin, agents that stimulate Ca2+ release from internal stores. In whole-cell recording from a slice preparation, light-evoked 'off' but not 'on' EPSCs in 'on-off' ganglion cells were reduced by 60 +/- 8% (n = 8, P < 0.01) by cytochalasin D. These data suggest that elevation of intracellular Ca2+ during excitatory synaptic activity initiates a cascade for activity-dependent actin remodelling, which in turn may serve as a feedback mechanism to attenuate excitotoxic Ca2+ accumulation induced by synaptic depolarization.

Indexed as

ActinsAlkaloidsAnimalsBenzophenanthridinesCalciumCalcium Channels, L-TypeCarcinogensCaudataCell SurvivalElectrophysiologyEnzyme InhibitorsGlutamic AcidIndolesMaleimidesNeurons, AfferentPhenanthridinesActinsAlkaloidsBenzophenanthridinesbisindolylmaleimide ICalciumCalcium Channels, L-TypeCarcinogenschelerythrineEnzyme InhibitorsGlutamic AcidIndolesMaleimidesPhenanthridinesPotassiumProtein Kinase CReceptors, GlutamateTetradecanoylphorbol Acetate

Identifiers

PMID16777935
PMCPMC1819466
OpenAlexW1488636309

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.