Evidence map›Paper›PMID 23785079›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2013

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats.

Javier E Stern, Evgeniy S Potapenko

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. Angiotensin II inhibits the A-type KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022
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  8. Review
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  13. Article
  14. Dendritic Release of Neurotransmitters.Comprehensive Physiology · 2016
    Review
  15. Article
  16. Multiple signalling modalities mediated by dendritic exocytosis of oxytocin and vasopressin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  17. 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 2 institutions in 1 country.

Javier E SternDepartment of Physiology, Georgia Regents University, Augusta, Georgia.
Evgeniy S Potapenko
Augusta University · USGeorgia Regents Medical Center · US

Funding

Altered CNS Intercellular Signaling Mechanisms in Cardiovascular DiseaseR01HL090948 · NHLBI · UNIVERSITY OF CINCINNATI · PI STERN, JAVIER E · 2008 to 2017
$3.0M
NHLBI NIH HHS R01 HL-090948
6 · The paper itself

Abstract

An enhanced glutamate excitatory function within the hypothalamic supraoptic and paraventricluar nuclei is known to contribute to increased neurosecretory and presympathetic neuronal activity, and hence, neurohumoral activation, during heart failure (HF). Still, the precise mechanisms underlying enhanced glutamate-driven neuronal activity in HF remain to be elucidated. Here, we performed simultaneous electrophysiology and fast confocal Ca²⁺ imaging to determine whether altered N-methyl-d-aspartate (NMDA) receptor-mediated changes in intracellular Ca²⁺ levels (NMDA-ΔCa²⁺) occurred in hypothalamic magnocellular neurosecretory cells (MNCs) in HF rats. We found that activation of NMDA receptors resulted in a larger ΔCa²⁺ in MNCs from HF when compared with sham rats. The enhanced NMDA-ΔCa²⁺ was neither dependent on the magnitude of the NMDA-mediated current (voltage clamp) nor on the degree of membrane depolarization or firing activity evoked by NMDA (current clamp). Differently from NMDA receptor activation, firing activity evoked by direct membrane depolarization resulted in similar changes in intracellular Ca²⁺ in sham and HF rats. Taken together, our results support a relatively selective alteration of intracellular Ca²⁺ homeostasis and signaling following activation of NMDA receptors in MNCs during HF. The downstream functional consequences of such altered ΔCa²⁺ signaling during HF are discussed.

Indexed as

Calcium SignalingAction PotentialsAnimalsDisease Models, AnimalExcitatory Amino Acid AgonistsFeedback, PhysiologicalHeart FailureHypothalamusMaleMicroscopy, ConfocalNeuronsN-MethylaspartatePatch-Clamp TechniquesRatsRats, WistarReceptors, N-Methyl-D-AspartateExcitatory Amino Acid AgonistsN-MethylaspartateReceptors, N-Methyl-D-AspartateCa2+glutamateNMDAsupraopticvasopressin

Identifiers

PMID23785079
PMCPMC3833393
OpenAlexW2160518146

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.