Evidence map›Paper›PMID 21255017›Full record

ArticleJournal of neurochemistry2011

Cytosolic zinc release and clearance in hippocampal neurons exposed to glutamate--the role of pH and sodium.

Lech Kiedrowski

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Metallothionein III Mediates CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Zinc Homeostasis in Platelet-Related Diseases.International journal of molecular sciences · 2019
    Review
  6. Article
  7. Intracellular ZnThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The neurophysiology and pathology of brain zinc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

1 author at 1 institution in 1 country.

Lech KiedrowskiDepartment of Psychiatry, The Psychiatric Institute, The University of Illinois at Chicago, Chicago, Illinois 60612, USA. lkiedr@psych.uic.edu
University of Illinois Chicago · US

Funding

Role of NCKX2 in the activation of toxic Zn2+ influx in ischemic neuronsR21NS065305 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KIEDROWSKI, LECH · 2009 to 2010
$392k
NINDS NIH HHS R21 NS065305
6 · The paper itself

Abstract

Although Zn(2+) homeostasis in neurons is tightly regulated and its destabilization has been linked to a number of pathologies including Alzheimer's disease and ischemic neuronal death, the primary mechanisms affecting intracellular Zn(2+) concentration ([Zn(2+) ](i)) in neurons exposed to excitotoxic stimuli remain poorly understood. The present work addressed these mechanisms in cultured hippocampal neurons exposed to glutamate and glycine (Glu/Gly). [Zn(2+)](i) and intracellular Ca(2+) concentration were monitored simultaneously using FluoZin-3 and Fura-2FF, and intracellular pH (pH(i)) was studied in parallel experiments using 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein. Glu/Gly applications under Na(+)-free conditions (Na(+) substituted with N-methyl-D-glucamine(+)) caused Ca(2+) influx, pH(i) drop, and Zn(2+) release from intracellular stores. Experimental maneuvers resulting in a pH(i) increase during Glu/Gly applications, such as stimulation of Na(+) -dependent pathways of H(+) efflux, forcing H(+) efflux via gramicidin-formed channels, or increasing extracellular pH counteracted [Zn(2+)](i) elevations. In the absence of Na(+), the rate of [Zn(2+)](i) decrease could be correlated with the rate of pH(i) increase. In the presence of Na(+), the rate of [Zn(2+) ](i) decrease was about twice as fast as expected from the rate of pH(i) elevation. The data suggest that Glu/Gly-induced cytosolic acidification promotes [Zn(2+) ](i) elevations and that Na(+) counteracts the latter by promoting pH(i)-dependent and pH(i)-independent mechanisms of cytosolic Zn(2+) clearance.

Indexed as

AnimalsCalciumCells, CulturedChelating AgentsCytosolDose-Response Relationship, DrugEdetic AcidEmbryo, MammalianEthylenediaminesExcitatory Amino Acid AgonistsFura-2Glutamic AcidGlycineHippocampusHydrogen-Ion ConcentrationMiceCalciumChelating AgentsEdetic AcidEthylenediaminesExcitatory Amino Acid AgonistsFluoZin-3Fura-2Glutamic AcidGlycineN-MethylaspartateN,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediaminePolycyclic CompoundsSodiumZinc

Identifiers

PMID21255017
PMCPMC3076735
OpenAlexW1494793612

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.