Evidence map›Paper›PMID 7666362›Full record

ArticleThe Journal of physiology1995

Thrombin-induced inhibition of potassium currents in human retinal glial (Müller) cells.

D G Puro, E L Stuenkel

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Thrombin induces CaMolecular vision · 2019
    Article
  3. Review
  4. Glial and neuronal dysfunction in streptozotocin-induced diabetic rats.Journal of ocular biology, diseases, and informatics · 2011
    Article
  5. Review
  6. ATP excites interneurons and astrocytes to increase synaptic inhibition in neuronal networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  7. Article
  8. Glial cell inhibition of neurons by release of ATP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  9. Article
  10. Article
  11. Energy metabolism in human retinal Müller cells.Investigative ophthalmology & visual science · 2000
    Article
  12. Article
  13. Article
  14. 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.

D G PuroDepartment of Opthalmology, University of Michigan, Ann-Arbor 48105, USA.
E L Stuenkel
University of Michigan · US

Funding

ION CHANNELS IN RETINAL GLIAL CELLSR01EY006931 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PURO, DONALD G · 1992 to 1999
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SODIUM REGULATION OF NEUROHORMONE SECRETIONR01NS031888 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STUENKEL, EDWARD L · 1993 to 1996
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PATCH CLAMP STUDIES OF MAMMALIAN RETINAL GLIAL CELLSR29EY006931 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PURO, DONALD G · 1987 to 1991
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NEI NIH HHS EY06931NEI NIH HHS EY07003NINDS NIH HHS NS31888
6 · The paper itself

Abstract

1. Glial cells are known to play a role in regulating the microenvironment of the nervous system. While earlier considerations of glial function assumed a passive, static physiology for these cells, this is not likely to be the case. In this study, we begin to examine how the physiology of Müller glial cells changes in response to molecules in the microenvironment. 2. Perforated-path recordings and intracellular calcium measurements were performed on human retinal Müller cells in vitro. 3. Analysis of whole-cell currents revealed that the human Müller glial cells have an inwardly rectifying K+ current (IK(IR) which is active near the resting membrane potential. This IK(IR) is significantly inhibited when the Müller cell is exposed to thrombin, a molecule that is likely to enter the retina with a breakdown of the blood-retinal barrier and may be endogenous to the nervous system. 4. A variety of experiments point to a role for Ca2+ as a second messenger mediating the inhibitory effect of thrombin on the IK(IR) of Müller cells. Specifically, thrombin evokes an increase in intracellular [Ca2+] in the Müller cells; the Ca2+ chelator BAPTA blocks the effects of thrombin on both the inhibition of IK(IR) and the rise in intracellular [Ca2+]; exposure to ionomycin, a calcium ionophore, induces a reduction in the IK(IR) of Müller cells. 5. A thrombin- induced inhibition in the IK(IR) of Müller cells is likely to have significant functional consequences for the retina since these ion channels are involved in K+ homeostasis. 6. Our experiments support the idea that the physiology of Müller glial cells is dynamic and can be markedly affected by molecules in the microenvironment.

Indexed as

BariumDepression, ChemicalEgtazic AcidFura-2HumansIn Vitro TechniquesIonomycinMembrane PotentialsNeurogliaPatch-Clamp TechniquesPotassium ChannelsRetinaThrombinVirulence Factors, Bordetella1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidBariumEgtazic AcidFura-2IonomycinPotassium ChannelsThrombinVirulence Factors, Bordetella

Identifiers

PMID7666362
PMCPMC1157996
OpenAlexW2012477788

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.