Evidence map›Paper›PMID 25315194›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2015

Enhanced dopamine-dependent hippocampal plasticity after single MK-801 application.

Julia C Bartsch, Pawel Fidzinski, Jojanneke H J Huck, Heide Hörtnagl, Richard Kovács, Agustin Liotta, Josef Priller, Christian Wozny, Joachim Behr

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 36% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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

9 authors at 2 institutions in 1 country.

Julia C Bartsch1] Department of Psychiatry and Psychotherapy, Charité - Universitätsmedizin Berlin, Berlin, Germany [2] Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Pawel Fidzinski1] Department of Psychiatry and Psychotherapy, Charité - Universitätsmedizin Berlin, Berlin, Germany [2] Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Jojanneke H J HuckDepartment of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Heide HörtnaglInstitute of Pharmacology and Toxicology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Richard KovácsInstitute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Agustin LiottaInstitute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Josef Priller1] Department of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité - Universitätsmedizin Berlin, Berlin, Germany [2] Cluster of Excellence NeuroCure, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Christian WoznyNeuroscience Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Joachim Behr1] Department of Psychiatry and Psychotherapy, Charité - Universitätsmedizin Berlin, Berlin, Germany [2] Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany [3] Department of Psychiatry and Psychotherapy, Ruppiner Kliniken, Neuruppin, Germany.
Charité - Universitätsmedizin Berlin · DEBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dopaminergic hyperfunction and N-methyl-D-aspartate receptor (NMDAR) hypofunction have both been implicated in psychosis. Dopamine-releasing drugs and NMDAR antagonists replicate symptoms associated with psychosis in healthy humans and exacerbate symptoms in patients with schizophrenia. Though hippocampal dysfunction contributes to psychosis, the impact of NMDAR hypofunction on hippocampal plasticity remains poorly understood. Here, we used an NMDAR antagonist rodent model of psychosis to investigate hippocampal long-term potentiation (LTP). We found that single systemic NMDAR antagonism results in a region-specific, presynaptic LTP at hippocampal CA1-subiculum synapses that is induced by activation of D1/D5 dopamine receptors and modulated by L-type voltage-gated Ca(2+) channels. Thereby, our findings may provide a cellular mechanism how NMDAR antagonism can lead to an enhanced hippocampal output causing activation of the hippocampus-ventral tegmental area-loop and overdrive of the dopamine system.

Indexed as

Adenylyl CyclasesAnimalsBicucullineCalciumCalcium Channel BlockersDizocilpine MaleateDopamineEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA-A Receptor AntagonistsGlutamic AcidHippocampusIn Vitro TechniquesLong-Term PotentiationMaleNifedipineAdenylyl CyclasesBicucullineCalciumCalcium Channel BlockersDizocilpine MaleateDopamineEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA-A Receptor AntagonistsGlutamic AcidNifedipine

Identifiers

PMID25315194
PMCPMC4330513
OpenAlexW2086505059

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.