Evidence map›Paper›PMID 12968005›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.

Elizabeth A Jonas, Daniel Hoit, John A Hickman, Teresa A Brandt, Brian M Polster, Yihru Fannjiang, Erin McCarthy, Marlena K Montanez, J Marie Hardwick, Leonard K Kaczmarek

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Physiological roles of the mitochondrial permeability transition pore.Journal of bioenergetics and biomembranes · 2017
    Review
  7. Review
  8. Bcl-xL Is Essential for the Survival and Function of Differentiated Neurons in the Cortex That Control Complex Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Review
  10. Review
  11. Bcl-xL in neuroprotection and plasticity.Frontiers in physiology · 2014
    Review
  12. Article
  13. Review
  14. Multiple functions of BCL-2 family proteins.Cold Spring Harbor perspectives in biology · 2013
    Review
  15. Article
  16. Prolonged expression of Puma in cholinergic amacrine cells during the development of rat retina.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012
    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

10 authors at 4 institutions in 1 country.

Elizabeth A JonasDepartment of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06250, USA.
Daniel Hoit
John A Hickman
Teresa A Brandt
Brian M Polster
Yihru Fannjiang
Erin McCarthy
Marlena K Montanez
J Marie Hardwick
Leonard K Kaczmarek
Mount Holyoke College · USWake Forest University · USYale University · USMarine Biological Laboratory · US

Funding

Biochemical Control of Excitibility in NeuronsR01NS018492 · NINDS · YALE UNIVERSITY · PI KACZMAREK, LEONARD K · 1985 to 2010
$3.6M
NOVEL GABA-A RECEPTOR SUBUNIT--PIR29NS034702 · NINDS · INSTITUTE FOR GENOMIC RESEARCH · PI KIRKNESS, EWEN · 1996 to 2000
$112k
NINDS NIH HHS NS 18492NINDS NIH HHS NS 34702NINDS NIH HHS R01 NS018492
6 · The paper itself

Abstract

BCL-2 family proteins are known to regulate cell death during development by influencing the permeability of mitochondrial membranes. The anti-apoptotic BCL-2 family protein BCL-xL is highly expressed in the adult brain and localizes to mitochondria in the presynaptic terminal of the adult squid stellate ganglion. Application of recombinant BCL-xL through a patch pipette to mitochondria inside the giant presynaptic terminal triggered multiconductance channel activity in mitochondrial membranes. Furthermore, injection of full-length BCL-xL protein into the presynaptic terminal enhanced postsynaptic responses and enhanced the rate of recovery from synaptic depression, whereas a recombinant pro-apoptotic cleavage product of BCL-xL attenuated postsynaptic responses. The effect of BCL-xL on synaptic responses persisted in the presence of a blocker of mitochondrial calcium uptake and was mimicked by injection of ATP into the terminal. These studies indicate that the permeability of outer mitochondrial membranes influences synaptic transmission, and they raise the possibility that modulation of mitochondrial conductance by BCL-2 family proteins affects synaptic stability.

Indexed as

Adenosine TriphosphateAnimalsbcl-X ProteinColoring AgentsDecapodiformesElectric StimulationIn Vitro TechniquesIon ChannelsLong-Term Synaptic DepressionMitochondriaNeuronsProto-Oncogene Proteins c-bcl-2Recovery of FunctionRuthenium RedSynaptic TransmissionAdenosine Triphosphatebcl-X ProteinColoring AgentsIon ChannelsProto-Oncogene Proteins c-bcl-2Ruthenium Red

Identifiers

PMID12968005
PMCPMC6740692
OpenAlexW2165983675

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.