Evidence map›Paper›PMID 20876360›Full record

ArticleThe Journal of general physiology2010

Neuroglial ATP release through innexin channels controls microglial cell movement to a nerve injury.

Stuart E Samuels, Jeffrey B Lipitz, Gerhard Dahl, Kenneth J Muller

Open access · greenAbstract read
In one paragraph

Article in The Journal of general physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 67 citations in OpenAlex.

  1. Circuit-constrained molecular neuroethology in the medicinal leech Hirudo verbana.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2026
    Review
  2. Article
  3. On the molecular nature of large-pore channels.Journal of molecular biology · 2021
    Review
  4. Article
  5. Review
  6. Article
  7. Glial Chloride Channels in the Function of the Nervous System Across Species.Advances in experimental medicine and biology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Inseparable tandem: evolution chooses ATP and Ca2+ to control life, death and cellular signalling.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  13. Review
  14. Review
  15. ATP release through pannexon channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  16. Article
  17. Mechanosensitive unpaired innexin channels in C. elegans touch neurons.American journal of physiology. Cell physiology · 2014
    Article
  18. Calreticulin contributes to C1q-dependent recruitment of microglia in the leech Hirudo medicinalis following a CNS injury.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Stuart E SamuelsNeuroscience Program, University of Miami School of Medicine, Miami, FL 33136, USA. SSamuels@med.miami.edu
Jeffrey B Lipitz
Gerhard Dahl
Kenneth J Muller
University of Miami · US

Funding

FORMATION OF CELL-CELL CHANNELSR01GM048610 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DAHL, GERHARD P · 1993 to 2010
$2.8M
Synapses,Channels, and Transduction in NeuroscienceT32NS007044 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MULLER, KENNETH J · 1985 to 2010
$2.2M
LOSS AND RESTORATION OF FUNCTION AFTER NEURONAL INJURYR01NS034927 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MULLER, KENNETH J · 1995 to 2007
$2.1M
TRAINING PROGRAM IN CNS INJURY AND REPAIRT32NS007459 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIETRICH, W DALTON · 2000 to 2009
$1.7M
NIGMS NIH HHS R01 GM048610NIGMS NIH HHS R01GM48610NINDS NIH HHS R01 NS034927NINDS NIH HHS R01NS034927NINDS NIH HHS T32 NS007044NINDS NIH HHS T32 NS007459
6 · The paper itself

Abstract

Microglia, the immune cells of the central nervous system, are attracted to sites of injury. The injury releases adenosine triphosphate (ATP) into the extracellular space, activating the microglia, but the full mechanism of release is not known. In glial cells, a family of physiologically regulated unpaired gap junction channels called innexons (invertebrates) or pannexons (vertebrates) located in the cell membrane is permeable to ATP. Innexons, but not pannexons, also pair to make gap junctions. Glial calcium waves, triggered by injury or mechanical stimulation, open pannexon/innexon channels and cause the release of ATP. It has been hypothesized that a glial calcium wave that triggers the release of ATP causes rapid microglial migration to distant lesions. In the present study in the leech, in which a single giant glial cell ensheathes each connective, hydrolysis of ATP with 10 U/ml apyrase or block of innexons with 10 µM carbenoxolone (CBX), which decreased injury-induced ATP release, reduced both movement of microglia and their accumulation at lesions. Directed movement and accumulation were restored in CBX by adding ATP, consistent with separate actions of ATP and nitric oxide, which is required for directed movement but does not activate glia. Injection of glia with innexin2 (Hminx2) RNAi inhibited release of carboxyfluorescein dye and microglial migration, whereas injection of innexin1 (Hminx1) RNAi did not when measured 2 days after injection, indicating that glial cells' ATP release through innexons was required for microglial migration after nerve injury. Focal stimulation either mechanically or with ATP generated a calcium wave in the glial cell; injury caused a large, persistent intracellular calcium response. Neither the calcium wave nor the persistent response required ATP or its release. Thus, in the leech, innexin membrane channels releasing ATP from glia are required for migration and accumulation of microglia after nerve injury.

Indexed as

Adenosine TriphosphateAnimalsCalcium SignalingCell MovementConnexinsLeechesMicrogliaNerve CrushNeurogliaOocytesRNA InterferenceTrauma, Nervous SystemXenopusAdenosine TriphosphateConnexins

Identifiers

PMID20876360
PMCPMC2947054
OpenAlexW2171855184

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.