Evidence map›Paper›PMID 26791526›Full record

ArticleNeuroscience2016

Activation of microglial P2Y12 receptor is required for outward potassium currents in response to neuronal injury.

P Swiatkowski, M Murugan, U B Eyo, Y Wang, S Rangaraju, S B Oh, L-J Wu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 78 citations in OpenAlex.

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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

7 authors at 4 institutions in 3 countries.

P SwiatkowskiDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, United States; Program in Cellular and Molecular Pharmacology, Rutgers University, Piscataway, NJ 08854, United States.
M MuruganDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, United States.
U B EyoDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, United States.
Y WangStomatological Hospital, Anhui Medical University, Hefei, Anhui 230032, China.
S RangarajuDepartment of Neurology, Emory University School of Medicine, 12 Executive Park Drive NE, Atlanta, GA 30329, United States.
S B OhDepartment of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, South Korea.
L-J WuDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, United States. Electronic address: lwu@dls.rutgers.edu.
Rutgers, The State University of New Jersey · USAnhui Medical University · CNEmory University · USSeoul National University · KR

Funding

TRAINING IN EVIRONMENTAL TOXICOLOGYT32ES007148 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Lauren M Aleksunes · 1987 to 2026
$11.4M
UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
The Role of Microglia in EpilepsyR01NS088627 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI WU, LONG-JUN · 2014 to 2023
$3.6M
NIEHS NIH HHS T32 ES007148NIEHS NIH HHS T32ES007148NIGMS NIH HHS T32 GM008339NIGMS NIH HHS T32GM8339NINDS NIH HHS R01 NS088627NINDS NIH HHS R01NS088627
6 · The paper itself

Abstract

Microglia, the resident immune cells in the central nervous system (CNS), constantly survey the surrounding neural parenchyma and promptly respond to brain injury. Activation of purinergic receptors such as P2Y12 receptors (P2Y12R) in microglia has been implicated in chemotaxis toward ATP that is released by injured neurons and astrocytes. Activation of microglial P2Y12R elicits outward potassium current that is associated with microglial chemotaxis in response to injury. This study aimed at investigating the identity of the potassium channel implicated in microglial P2Y12R-mediated chemotaxis following neuronal injury and understanding the purinergic signaling pathway coupled to the channel. Using a combination of two-photon imaging, electrophysiology and genetic tools, we found the ATP-induced outward current to be largely dependent on P2Y12R activation and mediated by G-proteins. Similarly, P2Y12R-coupled outward current was also evoked in response to laser-induced single neuron injury. This current was abolished in microglia obtained from mice lacking P2Y12R. Dissecting the properties of the P2Y12R-mediated current using a pharmacological approach revealed that both the ATP and neuronal injury-induced outward current in microglia was sensitive to quinine (1mM) and bupivacaine (400μM), but not tetraethylammonium (TEA) (10mM) and 4-aminopyridine (4-AP) (5mM). These results suggest that the quinine/bupivacaine-sensitive potassium channels are the functional effectors of the P2Y12R-mediated signaling in microglia activation following neuronal injury.

Indexed as

AnimalsAstrocytesCentral Nervous SystemFemaleMaleMembrane PotentialsMice, Inbred C57BLMicrogliaNeuronsPotassiumPotassium ChannelsReceptors, Purinergic P2Y12Signal TransductionP2ry12 protein, mousePotassiumPotassium ChannelsReceptors, Purinergic P2Y12ATPK(+) channelsmicrogliaP2Y12 receptor

Identifiers

PMID26791526
PMCPMC4753827
OpenAlexW2287801381

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.