Evidence map›Paper›PMID 20392936›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Cholecystokinin facilitates glutamate release by increasing the number of readily releasable vesicles and releasing probability.

Pan-Yue Deng, Zhaoyang Xiao, Archana Jha, David Ramonet, Toshimitsu Matsui, Michael Leitges, Hee-Sup Shin, James E Porter, Jonathan D Geiger, Saobo Lei

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. 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
3.2field-weighted citation impact, top 8% 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, 70 citations in OpenAlex.

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  13. Visuoauditory Associative Memory Established with Cholecystokinin Under Anesthesia Is Retrieved in Behavioral Contexts.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  14. Review
  15. Roles of KNeuropharmacology · 2019
    Article
  16. Article
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  19. Article
  20. Postsynaptic Depolarization Enhances GABA Drive to Dorsomedial Hypothalamic Neurons through Somatodendritic Cholecystokinin Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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 4 countries.

Pan-Yue DengDepartment of Pharmacology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota 58203, USA.
Zhaoyang Xiao
Archana Jha
David Ramonet
Toshimitsu Matsui
Michael Leitges
Hee-Sup Shin
James E Porter
Jonathan D Geiger
Saobo Lei
University of North Dakota · USKobe University · JPKorea Institute of Science and Technology · KRUniversity of Oslo · NO

Funding

Roles and mechanisms of neurotensin in learning and memoryR01MH082881 · NIMH · UNIVERSITY OF NORTH DAKOTA · PI LEI, SAOBO · 2008 to 2015
$2.5M
NIMH NIH HHS R01 MH082881NIMH NIH HHS R01MH082881
6 · The paper itself

Abstract

Cholecystokinin (CCK), a neuropeptide originally discovered in the gastrointestinal tract, is abundantly distributed in the mammalian brains including the hippocampus. Whereas CCK has been shown to increase glutamate concentration in the perfusate of hippocampal slices and in purified rat hippocampal synaptosomes, the cellular and molecular mechanisms whereby CCK modulates glutamatergic function remain unexplored. Here, we examined the effects of CCK on glutamatergic transmission in the hippocampus using whole-cell recordings from hippocampal slices. Application of CCK increased AMPA receptor-mediated EPSCs at perforant path-dentate gyrus granule cell, CA3-CA3 and Schaffer collateral-CA1 synapses without effects at mossy fiber-CA3 synapses. CCK-induced increases in AMPA EPSCs were mediated by CCK-2 receptors and were not modulated developmentally and transcriptionally. CCK reduced the coefficient of variation and paired-pulse ratio of AMPA EPSCs suggesting that CCK facilitates presynaptic glutamate release. CCK increased the release probability and the number of readily releasable vesicles with no effects on the rate of recovery from vesicle depletion. CCK-mediated increases in glutamate release required the functions of phospholipase C, intracellular Ca(2+) release and protein kinase Cgamma. CCK released endogenously from hippocampal interneurons facilitated glutamatergic transmission. Our results provide a cellular and molecular mechanism to explain the roles of CCK in the brain.

Indexed as

AnimalsCalciumCholecystokininExcitatory Postsynaptic Potentialsgamma-Aminobutyric AcidGlutamic AcidHippocampusIntracellular SpaceIn Vitro TechniquesNeuronsPotassium ChannelsPresynaptic TerminalsProbabilityProtein Kinase CRatsRats, Sprague-DawleyCalciumCholecystokiningamma-Aminobutyric AcidGlutamic AcidPotassium ChannelsProtein Kinase Cprotein kinase C gammaReceptor, Cholecystokinin BReceptors, AMPAType C Phospholipases

Identifiers

PMID20392936
PMCPMC3073615
OpenAlexW2067024887

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.