Evidence map›Paper›PMID 26453330›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Purinergic glio-endothelial coupling during neuronal activity: role of P2Y1 receptors and eNOS in functional hyperemia in the mouse somatosensory cortex.

Peter Toth, Stefano Tarantini, Antonio Davila, M Noa Valcarcel-Ares, Zsuzsanna Tucsek, Behzad Varamini, Praveen Ballabh, William E Sonntag, Joseph A Baur, Anna Csiszar and 1 more

Registry-linked trialAbstract read
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In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07651787 (Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment), which is not on this map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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.

NCT07651787 narecruitingnot on this mapstarted 2025, after this paper: background citation

Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment

TypeinterventionalSponsorUniversity of OklahomaRan2025 to 2026Enrolled40ConditionsMild Cognitive Impairment (MCI), Amyloid PathologyArmsActive Vielight Neuro RX-Duo device -Active transcranial photobiomodulation, Sham Vielight Neuro RX-Duo device -Sham transcranial photobiomodulation
3 · Its place in the literature

Who cites it

64 citing papers in PubMed.

  1. Review
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  9. Disease-relevant upregulation of P2YNature communications · 2024
    Article
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  20. Cerebral arteriolar and neurovascular dysfunction after chemically induced menopause in mice.American journal of physiology. Heart and circulatory physiology · 2022
    Article

4 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

11 authors.

Peter TothReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Department of Neurosurgery, University of Pecs, Pecs, Hungary; Szentagothai Research Center, Medical School, University of Pecs, Pecs, Hungary;
Stefano TarantiniReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma;
Antonio DavilaInstitute for Diabetes, Obesity, and Metabolism and Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania;
M Noa Valcarcel-AresReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma;
Zsuzsanna TucsekReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Szentagothai Research Center, Medical School, University of Pecs, Pecs, Hungary;
Behzad VaraminiBiological Sciences Department, Biola University, La Mirada, California;
Praveen BallabhDepartment of Cell Biology and Anatomy, New York Medical College, Valhalla, New York; Department of Pediatrics, Regional Neonatal Center, Maria Fareri Children's Hospital at Westchester Medical Center, New York Medical College, Valhalla, New York;
William E SonntagReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; The Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Joseph A BaurInstitute for Diabetes, Obesity, and Metabolism and Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania;
Anna CsiszarReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Szentagothai Research Center, Medical School, University of Pecs, Pecs, Hungary; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; The Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Zoltan UngvariReynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Szentagothai Research Center, Medical School, University of Pecs, Pecs, Hungary; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; The Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma zoltan-ungvari@ouhsc.edu.

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI DOUGLAS J EPSTEIN · 1986 to 2026
$48.3M
Targeting NAD Metabolism to Improve Glucose Homeostasis in Obesity and AgingR01DK098656 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Joseph A. Baur · 2013 to 2026
$6.1M
RESOURCE CORE 3: ANALYTICAL COREP30AG028718 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI WEI, JEANNE Y · 2011 to 2015
$5.1M
Effects of Radiation on Brain Microvasculature and CognitionR01NS056218 · NINDS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CSISZAR, ANNA, SONNTAG, WILLIAM EDMUND · 2007 to 2018
$3.6M
NOVEL APPROACHES FOR REGULATION OF IGF-1 LEVELS THROUGHOUT THE LIFESPANR01AG038747 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SONNTAG, WILLIAM EDMUND · 2011 to 2015
$2.4M
Molecular Mechanisms of Rapamycin's Effects on Health and LongevityR01AG043483 · NIA · UNIVERSITY OF PENNSYLVANIA · PI BAUR, JOSEPH A. · 2013 to 2017
$2.0M
Role of SIRT1 in vasoprotectionR01AT006526 · NCCIH · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI UNGVARI, ZOLTAN ISTVAN · 2010 to 2014
$1.8M
Microvascular mechanisms of neuroinflammation: role of Nrf2R01AG047879 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CSISZAR, ANNA · 2014 to 2018
$1.5M
Does SIRT1 regulate mammalian health and longevity?R00AG031182 · NIA · UNIVERSITY OF PENNSYLVANIA · PI BAUR, JOSEPH A. · 2009 to 2011
$732k
NCCIH NIH HHS R01-AT006526NIA NIH HHS P30 AG028718NIA NIH HHS R00-AG031182NIA NIH HHS R01-AG038747NIA NIH HHS R01 AG043483NIA NIH HHS R01-AG043483NIA NIH HHS R01 AG047879NIA NIH HHS R01-AG047879NIDDK NIH HHS P30-DK19525NIDDK NIH HHS R01 DK098656NIDDK NIH HHS R01-DK098656NINDS NIH HHS R01-NS056218
6 · The paper itself

Abstract

Impairment of moment-to-moment adjustment of cerebral blood flow (CBF) via neurovascular coupling is thought to play a critical role in the genesis of cognitive impairment associated with aging and pathological conditions associated with accelerated cerebromicrovascular aging (e.g., hypertension, obesity). Although previous studies demonstrate that endothelial dysfunction plays a critical role in neurovascular uncoupling in these conditions, the role of endothelial NO mediation in neurovascular coupling responses is not well understood. To establish the link between endothelial function and functional hyperemia, neurovascular coupling responses were studied in mutant mice overexpressing or deficient in endothelial NO synthase (eNOS), and the role of P2Y1 receptors in purinergic glioendothelial coupling was assessed. We found that genetic depletion of eNOS (eNOS(-/-)) and pharmacological inhibition of NO synthesis significantly decreased the CBF responses in the somatosensory cortex evoked by whisker stimulation and by administration of ATP. Overexpression of eNOS enhanced NO mediation of functional hyperemia. In control mice, the selective and potent P2Y1 receptor antagonist MRS2179 attenuated both whisker stimulation-induced and ATP-mediated CBF responses, whereas, in eNOS(-/-) mice, the inhibitory effects of MRS2179 were blunted. Collectively, our findings provide additional evidence for purinergic glio-endothelial coupling during neuronal activity, highlighting the role of ATP-mediated activation of eNOS via P2Y1 receptors in functional hyperemia.

Indexed as

Cell CommunicationMicrocirculationNeurovascular CouplingAnimalsAstrocytesEndothelial CellsEnzyme InhibitorsHemodynamicsHomeostasisHyperemiaMechanotransduction, CellularMice, Inbred C57BLMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIPurinergic P2Y Receptor AgonistsEnzyme InhibitorsNitric OxideNitric Oxide Synthase Type IIINos3 protein, mouseP2ry1 protein, mousePurinergic P2Y Receptor AgonistsPurinergic P2Y Receptor AntagonistsReceptors, Purinergic P2Y1astrocytedementiaendothelial dysfunctionendothelial nitric oxide synthaseendotheliumvascular cognitive impairment

Identifiers

PMID26453330
PMCPMC4698379

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Registered trials

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.