Evidence map›Paper›PMID 25475355›Full record

ArticleJournal of neurophysiology2015

Glutamate receptors in the hypothalamic paraventricular nucleus contribute to insulin-induced sympathoexcitation.

Sean D Stocker, Kathryn W Gordon

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2015. 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
1.0field-weighted citation impact, top 28% 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, 26 citations in OpenAlex.

  1. Role of the carotid chemoreceptors in insulin-mediated sympathoexcitation in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Trial
  2. Review
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  4. Article
  5. Review
  6. Obesity: sex and sympathetics.Biology of sex differences · 2020
    Review
  7. Sites and sources of sympathoexcitation in obese male rats: role of brain insulin.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Hypothalamic signaling mechanisms in hypertension.Current hypertension reports · 2015
    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

2 authors at 1 institution in 1 country.

Sean D StockerDepartment of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania; and Department of Neural and Behavioral Neuroscience, Pennsylvania State College of Medicine, Hershey, Pennsylvania sstocker@hmc.psu.edu.
Kathryn W GordonDepartment of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania; and.
Penn State Milton S. Hershey Medical Center · US

Funding

Central Nervous System Mechanisms of Obesity HypertensionR01HL090826 · NHLBI · UNIVERSITY OF KENTUCKY · PI STOCKER, SEAN D · 2008 to 2012
$1.9M
Central Osmosensory Mechanisms in Salt-Sensitive HypertensionR01HL113270 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STOCKER, SEAN D · 2013 to 2016
$1.5M
NHLBI NIH HHS HL-090826NHLBI NIH HHS HL-113270NHLBI NIH HHS R01 HL090826NHLBI NIH HHS R01 HL113270
6 · The paper itself

Abstract

The sympathoexcitatory response to insulin is mediated by neurons in the arcuate nucleus (ARC) and hypothalamic paraventricular nucleus (PVH). Previous studies have reported that stimulation of ARC neurons increases sympathetic nerve activity (SNA) and arterial blood pressure (ABP) through glutamate receptor activation in the PVH. Therefore, the purpose of the present study was to determine whether glutamatergic neurotransmission in the PVH contributes to insulin-induced sympathoexcitation. Male Sprague-Dawley rats (275-400 g) were infused with isotonic saline or insulin (3.75 mU · kg(-1) · min(-1)) plus 50% dextrose to maintain euglycemia. Intravenous infusion of insulin significantly increased lumbar SNA without a significant change in mean ABP, renal SNA, heart rate, or blood glucose. Bilateral PVH injection of the excitatory amino acid antagonist kynurenic acid (KYN) lowered lumbar SNA and ABP of animals infused with insulin. Similarly, a cocktail of the NMDA antagonist DL-2-amino-5-phosphonopentanoic acid (AP5) and non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) reduced lumbar SNA and mean ABP during infusion of insulin. In a final experiment, bilateral PVH injection of AP5 only, but not CNQX, lowered lumbar SNA and mean ABP of animals infused with insulin. The peak changes in lumbar SNA and mean ABP of insulin-treated animals were not different between KYN, AP5 plus CNQX, or AP5 alone. These drug treatments did not alter any variable in animals infused with saline. Altogether, these findings suggest that glutamatergic NMDA neurotransmission in the PVH contributes to insulin-induced sympathoexcitation.

Indexed as

Excitatory Postsynaptic PotentialsAnimalsBlood GlucoseExcitatory Amino Acid AntagonistsInsulinMaleNeuronsParaventricular Hypothalamic NucleusRatsRats, Sprague-DawleyReceptors, GlutamateSympathetic Nervous SystemBlood GlucoseExcitatory Amino Acid AntagonistsInsulinReceptors, Glutamateblood pressurehypothalamuslumbarNMDAsympathetic nerve activity

Identifiers

PMID25475355
PMCPMC4346732
OpenAlexW2081765499

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.