Evidence map›Paper›PMID 14985918›Full record

ArticlePsychopharmacology2004

NMDA receptor subunit and CaMKII changes in rat hippocampus induced by acute MDMA treatment: a mechanism for learning impairment.

S Moyano, D Frechilla, J Del Río

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In one paragraph

Article in Psychopharmacology, 2004. 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
2.3field-weighted citation impact, top 12% 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, 47 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Article
  5. Endogenous serotonin facilitates hippocampal long-term potentiation at CA3/CA1 synapses.Journal of neural transmission (Vienna, Austria : 1996) · 2015
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  7. 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

3 authors at 1 institution in 1 country.

S MoyanoDepartment of Pharmacology, School of Medicine, University of Navarra, Apartado 177, 31080 Pamplona, Spain.
D Frechilla
J Del Río
Universidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleCognitive deficits have been reported in recreational 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") users. In rats and other animal species, acute MDMA administration produces an impairment in passive avoidance and other learning tasks. Different studies have shown that this learning deficit is not strictly related to the pronounced serotonin (5-HT) depletion induced by the drug.

objectivesThis study was aimed at determining if acute MDMA administration induces in the rat hippocampus early molecular changes related to memory impairment in a passive avoidance task. The membrane expression of key molecules in memory consolidation, such as the NR1 and NR2B subunits of the N-methyl-D-aspartate (NMDA) receptor, Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein phosphatase 1 (PP1) was measured. Some of these studies were also performed after 5-HT depletion induced by the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA).

methodsNeurochemical studies were performed in rats treated with MDMA and killed 90 min later and also in rats subjected to passive avoidance 30 min after MDMA treatment. Western blotting was used for measuring the levels of NMDA receptor subunits, CAMKII and PP1. Enzyme activity assays were also performed.

resultsIn hippocampal membrane extracts, passive avoidance training increased NMDA receptor NR1 subunit expression as well as CaMKII levels and phosphorylated CaMKII. In untrained rats, MDMA reduced NR1 and NR2B protein levels, membrane CaMKII levels and enzyme activity, and enhanced PP1 levels and activity. In trained rats, MDMA prevented the learning-specific increase in NR1 subunit expression and membrane CaMKII/pCaMKII levels. After pronounced 5-HT depletion by PCPA, MDMA impaired passive avoidance retention to a similar extent and also prevented the training-associated changes in NR1 levels and CaMKII activity.

conclusionsDiminished function of hippocampal CaMKII and reduced levels of synaptic NMDA receptor subunits appear to be involved in the impairment of passive avoidance learning induced in rats by acute MDMA treatment.

Indexed as

AnimalsAvoidance LearningCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2FenclonineHippocampusMaleN-Methyl-3,4-methylenedioxyamphetaminePhosphoprotein PhosphatasesProtein Phosphatase 1Protein SubunitsRatsRats, WistarReceptors, N-Methyl-D-AspartateSerotoninSerotonin AgentsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2FenclonineN-Methyl-3,4-methylenedioxyamphetamineNR1 NMDA receptorNR2B NMDA receptorPhosphoprotein PhosphatasesProtein Phosphatase 1Protein SubunitsReceptors, N-Methyl-D-AspartateSerotoninSerotonin AgentsSerotonin Antagonists

Identifiers

PMID14985918
OpenAlexW2082109742

What OpenQuestion holds

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Registered trials

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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.