Evidence map›Paper›PMID 11978812›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Phosphatidylinositol 3-kinase is required for the expression but not for the induction or the maintenance of long-term potentiation in the hippocampal CA1 region.

Pietro Paolo Sanna, Maurizio Cammalleri, Fulvia Berton, Cindy Simpson, Robert Lutjens, Floyd E Bloom, Walter Francesconi

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 251 citations in OpenAlex.

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  11. Insulin and Insulin Resistance in Alzheimer's Disease.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Baicalin ameliorates chronic mild stress-induced depression-like behaviors in mice and attenuates inflammatory cytokines and oxidative stress.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Mice Deficient inMolecular and cellular biology · 2017
    Article
  20. Article

58 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Pietro Paolo SannaDepartment of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA. psanna@scripps.edu
Maurizio Cammalleri
Fulvia Berton
Cindy Simpson
Robert Lutjens
Floyd E Bloom
Walter Francesconi
Scripps Research Institute · USUniversity of Pisa · IT

Funding

SYSTEMIC NEUROPHARMACOLOGYP50AA006420 · NIAAA · SCRIPPS RESEARCH INSTITUTE · PI KOOB, GEORGE F · 1985 to 2002
$5.1M
Cellular Mechanisms of HIV-induced Cognitive DeficitsR21MH064376 · NIMH · SCRIPPS RESEARCH INSTITUTE · PI SANNA, PIETRO P · 2001 to 2003
$685k
PI3-KINASE IN SYNAPTIC PLASTICITYR03MH062140 · NIMH · SCRIPPS RESEARCH INSTITUTE · PI SANNA, PIETRO P · 2000 to 2001
$177k
NIAAA NIH HHS P50 AA006420NIAAA NIH HHS P50AA06420NIMH NIH HHS MH62140NIMH NIH HHS MH64376NIMH NIH HHS R21 MH064376
6 · The paper itself

Abstract

Several signal transduction pathways have been implicated in the induction of long-term potentiation (LTP), yet the signal transduction mechanisms behind the maintenance-expression phase of LTP are still poorly understood. We investigated the role of phosphatidylinositol 3-kinase (PI3-kinase) in LTP at Schaffer collateral/commissural fiber-CA1 synapses in rat hippocampal slices using biochemical approaches and extracellular electrophysiological recordings. We observed that PI3-kinase activity was induced in the CA1 region during LTP of field EPSPs (fEPSPs) and that two structurally unrelated PI3-kinase inhibitors, LY294002 and wortmannin, abated established LTP, suggesting that PI3-kinase is involved in the maintenance-expression phase of LTP. However, LTP recovered after washout of the reversible PI3-kinase inhibitor LY294002, confirming that LTP maintenance and expression are distinct events and indicating that PI3-kinase activity is required for LTP expression rather than for its maintenance. Interestingly, preincubation with LY294002 did not prevent LTP induction. In fact, if LY294002 was withdrawn 5 min after high-frequency stimulation, an LTP of fEPSP was seen. Last, a voltage-dependent calcium channel-dependent form of LTP in the CA1 could also be reversibly abated by LY294002, raising the possibility that PI3-kinase could be required for the expression of multiple forms of synaptic potentiation.

Indexed as

Protein Serine-Threonine KinasesAndrostadienesAnimalsCalcium Channel BlockersCalcium ChannelsChromonesElectric StimulationEnzyme ActivationEnzyme InhibitorsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGABA AntagonistsHippocampusIn Vitro TechniquesLong-Term PotentiationMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAndrostadienesCalcium Channel BlockersCalcium ChannelsChromonesEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA AntagonistsMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 KinasesWortmannin

Identifiers

PMID11978812
PMCPMC6758361
OpenAlexW2128134322

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.