Evidence map›Paper›PMID 8815877›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996

Induction of hippocampal long-term depression requires release of Ca2+ from separate presynaptic and postsynaptic intracellular stores.

M Reyes, P K Stanton

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 184 citations in OpenAlex.

  1. Article
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  8. Organelle-Specific Sensors for Monitoring CaFrontiers in synaptic neuroscience · 2016
    Review
  9. Article
  10. Article
  11. Incorporation of inwardly rectifying AMPA receptors at silent synapses during hippocampal long-term potentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Article
  12. Long-term depression: a cell biological view.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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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.

M ReyesDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461-1602, USA.
P K Stanton
Albert Einstein College of Medicine · US

Funding

MINORITY PREDOCTORAL FELLOWSHIP PROGRAM - NIGMSF31GM016379 · NIGMS · YESHIVA UNIVERSITY · PI REYES, MAGALI · 1993 to 1997
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NIGMS NIH HHS F31 GM016379NIGMS NIH HHS F31GM16379PHS HHS 45752
6 · The paper itself

Abstract

Studies have suggested that an increase in intracellular [Ca2+] is necessary for the induction of both long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission, and that release of Ca2+ from intracellular storage pools can be necessary to induce LTP. We investigated whether release of Ca2+ from intracellular stores also is required for the induction of LTD at Schaffer collateral-CA1 synapses in hippocampal slices. Both thapsigargin (1 microM) and cyclopiazonic acid (1 microM), compounds that deplete all intracellular Ca2+ pools by blocking LTP-dependent Ca2+ uptake into intracellular compartments, blocked the induction, but not maintenance, of LTD by low-frequency stimulation (LFS) (1 Hz/15 min) without affecting baseline synaptic transmission. Washout of the reversible inhibitor cyclopiazonic acid restored the ability to induce LTD. In contrast, thapsigargin did not block depotentiation of LTP by 1 Hz LFS, suggesting that LTP causes a reduction in the threshold [Ca2+] necessary for LTD. Selective depletion of the ryanodine receptor-gated Ca2+ pool by bath application of ryanodine (10 microM) also blocked the induction of LTD, indicating a requirement for Ca(2+)-induced Ca2+ release. Impalement of CA1 pyramidal neurons with microelectrodes containing thapsigargin (500 nM to 200 microM) prevented the induction of LTD at synapses on that neuron without blocking LTD in the rest of the slice. In contrast, similar filling of CA1 pyramidal neurons with ryanodine (2 microM to 5 mM) did not block the induction of LTD. From these data, we conclude that the induction of LTD requires release of Ca2+ both from a presynaptic ryanodine-sensitive pool and from postsynaptic (presumably IP3-gated) stores.

Indexed as

Long-Term PotentiationAnimalsCalciumEnzyme InhibitorsHippocampusIndolesIntracellular MembranesIn Vitro TechniquesMalePresynaptic TerminalsRatsRats, Sprague-DawleyRyanodineSynapsesThapsigarginCalciumcyclopiazonic acidEnzyme InhibitorsIndolesRyanodineThapsigargin

Identifiers

PMID8815877
PMCPMC6579182
OpenAlexW1589881202

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.