Evidence map›Paper›PMID 11306608›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Calcium-dependent inhibition of L, N, and P/Q Ca2+ channels in chromaffin cells: role of mitochondria.

J M Hernandez-Guijo, V E Maneu-Flores, A Ruiz-Nuno, M Villarroya, A G Garcia, L Gandia

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 73 citations in OpenAlex.

  1. Mitochondrial CaBiomolecules · 2026
    Review
  2. Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023
    Review
  3. Article
  4. L-type calcium channels in exocytosis and endocytosis of chromaffin cells.Pflugers Archiv : European journal of physiology · 2018
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Regulation by L-type calcium channels of endocytosis: an overview.Journal of molecular neuroscience : MN · 2012
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Mitochondria and Ca(2+) signaling: old guests, new functions.Pflugers Archiv : European journal of physiology · 2007
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

J M Hernandez-GuijoInstituto Teófilo Hernando, Departamento de Farmacología, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain.
V E Maneu-Flores
A Ruiz-Nuno
M Villarroya
A G Garcia
L Gandia
Universidad Autónoma de Madrid · ESHospital Universitario de La Princesa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hypothesis that the buffering of Ca(2+) by mitochondria could affect the Ca(2+)-dependent inhibition of voltage-activated Ca(2+) channels, (I(Ca)), was tested in voltage-clamped bovine adrenal chromaffin cells. The protonophore carbonyl cyanide m-chlorophenyl-hydrazone (CCCP), the blocker of the Ca(2+) uniporter ruthenium red (RR), and a combination of oligomycin plus rotenone were used to interfere with mitochondrial Ca(2+) buffering. In cells dialyzed with an EGTA-free solution, peak I(Ca) generated by 20 msec pulses to 0 or +10 mV, applied at 15 sec intervals, from a holding potential of -80 mV, decayed rapidly after superfusion of cells with 2 microm CCCP (tau = 16.7 +/- 3 sec; n = 8). In cells dialyzed with 14 mm EGTA, CCCP did not provoke I(Ca) loss. Cell dialysis with 4 microm ruthenium red or cell superfusion with oligomycin (3 microm) plus rotenone (4 microm) also accelerated the decay of I(Ca). After treatment with CCCP, decay of N- and P/Q-type Ca(2+) channel currents occurred faster than that of L-type Ca(2+) channel currents. These data are compatible with the idea that the elevation of the bulk cytosolic Ca(2+) concentration, [Ca(2+)](c), causes the inhibition of L- and N- as well as P/Q-type Ca(2+) channels expressed by bovine chromaffin cells. This [Ca(2+)](c) signal appears to be tightly regulated by rapid Ca(2+) uptake into mitochondria. Thus, it is plausible that mitochondria might efficiently regulate the activity of L, N, and P/Q Ca(2+) channels under physiological stimulation conditions of the cell.

Indexed as

AnimalsCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCarbonyl Cyanide m-Chlorophenyl HydrazoneCattleCells, CulturedChelating AgentsChromaffin CellsIntracellular FluidIonophoresMitochondriaCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCarbonyl Cyanide m-Chlorophenyl HydrazoneChelating AgentsIonophoresOligomycinsReceptors, NicotinicRotenoneRuthenium RedSodium Channels

Identifiers

PMID11306608
PMCPMC6762545
OpenAlexW2143716304

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.