Evidence map›Paper›PMID 22763616›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012

Altered acquisition and extinction of amphetamine-paired context conditioning in genetic mouse models of altered NMDA receptor function.

Michael A Benneyworth, Joseph T Coyle

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Integrating human brain proteomic data with genome-wide association study findings identifies novel brain proteins in substance use traits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
  5. Article
  6. Serine Racemase Expression by Striatal Neurons.Cellular and molecular neurobiology · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. The Role of Serine Racemase in the Pathophysiology of Brain Disorders.Advances in pharmacology (San Diego, Calif.) · 2018
    Review
  11. Article
  12. Multiple risk pathways for schizophrenia converge in serine racemase knockout mice, a mouse model of NMDA receptor hypofunction.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

2 authors at 2 institutions in 1 country.

Michael A BenneyworthDepartment of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, MA, USA.
Joseph T Coyle
Harvard University · USMcLean Hospital · US

Funding

NMDA RECEPTOR FUNCTION IN SCHIZOPHRENIAP50MH060450 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 2000 to 2010
$15.4M
PSYCHOSIS AND BRAIN GLUTAMATER01MH051290 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI COYLE, JOSEPH T. · 1994 to 2017
$5.0M
NIMH NIH HHS P50 MH060450NIMH NIH HHS P50MH0G0450NIMH NIH HHS R01 MH051290NIMH NIH HHS R01MH05190
6 · The paper itself

Abstract

Repeated intermittent exposure to amphetamine (AMPH) results in the development of persistent behavioral and neurological changes. When drug exposure is paired with a specific environment, contextual cues can control conditioned responses, context-specific sensitization, and alterations in dendritic morphology in the nucleus accumbens (NAc). Intact N-methyl-D-aspartate (NMDA) glutamate receptor signaling is thought to be required for associative learning. The acquisition of context-specific behavioral sensitization to AMPH and extinction of conditioned hyperactivity have been investigated in two genetically modified mouse strains: the serine racemase homozygous knockout (SR-/-) and glycine transporter 1 heterozygous mutant (GlyT1-/+). These strains have reciprocally altered NMDA receptor co-agonists, D-serine and glycine, levels that result in decreased (SR-/-) or increased (GlyT1-/+) NMDA receptor signaling. AMPH-induced changes in dendritic morphology in the NAc were also examined. SR-/- mice showed reduced expression of context-specific sensitization and conditioned hyperactivity. However, the conditioned hyperactivity in these mice is completely resistant to extinction. Extinction reversed AMPH-induced increased in NAc spine density in wild-type but not SR-/- mice. GlyT1 -/+ mice showed a more rapid acquisition of sensitization, but no alteration in the extinction of conditioned hyperactivity. The SR-/- data demonstrate that a genetic model of NMDA receptor hypofunction displays a reduced ability to extinguish conditioned responses to drug-associated stimuli. Findings also demonstrate that the morphological changes in the NAc encode conditioned responses that are sensitive to extinction and reduced NMDA receptor activity. NMDA receptor hypofunction may contribute to the comorbidity of substance abuse in schizophrenia.

Indexed as

AmphetamineAnalysis of VarianceAnimalsBehavioral SymptomsCentral Nervous System StimulantsConditioning, PsychologicalCuesDendritic SpinesDose-Response Relationship, DrugExtinction, PsychologicalGlycine Plasma Membrane Transport ProteinsHyperkinesisL-Serine DehydrataseMiceMice, Inbred C57BLMice, TransgenicAmphetamineCentral Nervous System StimulantsGlycine Plasma Membrane Transport ProteinsL-Serine DehydrataseReceptors, N-Methyl-D-AspartateSlc6a9 protein, mouse

Identifiers

PMID22763616
PMCPMC3442344
OpenAlexW2122907015

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.