Evidence map›Paper›PMID 19439608›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Prenatal cocaine reduces AMPA receptor synaptic expression through hyperphosphorylation of the synaptic anchoring protein GRIP.

Kalindi Bakshi, Serena Gennaro, Christopher Y Chan, Mary Kosciuk, Jingjing Liu, Andres Stucky, Ekkehart Trenkner, Eitan Friedman, Robert G Nagele, Hoau-Yan Wang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Glutamate receptors in brain development.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021
    Review
  2. Review
  3. Article
  4. Cocaine-induced neurodevelopmental deficits and underlying mechanisms.Birth defects research. Part C, Embryo today : reviews · 2016
    Review
  5. Article
  6. Activity-dependent synaptic GRIP1 accumulation drives synaptic scaling up in response to action potential blockade.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  7. Disruption of glutamate receptor-interacting protein in nucleus accumbens enhances vulnerability to cocaine relapse.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
    Article
  8. Article
  9. Coupling mechanical forces to electrical signaling: molecular motors and the intracellular transport of ion channels.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2013
    Review
  10. Article
  11. Article
  12. Cortical development of AMPA receptor trafficking proteins.Frontiers in molecular neuroscience · 2012
    Article
  13. Article
  14. Article
  15. 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 3 institutions in 2 countries.

Kalindi BakshiDepartment of Physiology, The City University of New York Medical School, New York, New York 10031, USA.
Serena Gennaro
Christopher Y Chan
Mary Kosciuk
Jingjing Liu
Andres Stucky
Ekkehart Trenkner
Eitan Friedman
Robert G Nagele
Hoau-Yan Wang
City University of New York · USRowan University · USNew York Medical College · US

Funding

MIDARP at CCNYR24DA018055 · NIDA · CITY COLLEGE OF NEW YORK · PI FRIEDMAN, EITAN · 2005 to 2010
$2.2M
NIDA NIH HHS R24 DA018055
6 · The paper itself

Abstract

Prenatal cocaine exposure produces sustained neurobehavioral and brain synaptic changes closely resembling those of animals with defective AMPA receptors (AMPARs). We hypothesized that prenatal cocaine exposure attenuates AMPAR signaling by interfering with AMPAR synaptic targeting. AMPAR function is governed by receptor cycling on and off the synaptic membrane through its interaction with glutamate receptor-interacting protein (GRIP), a PDZ domain protein that is regulated by reversible phosphorylation. Our results show that prenatal cocaine exposure markedly reduces AMPAR synaptic targeting and attenuates AMPAR-mediated synaptic long-term depression in the frontal cortex of 21-d-old rats. This cocaine effect is the result of reduced GRIP-AMPAR interaction caused by persistent phosphorylation of GRIP by protein kinase C (PKC) and Src tyrosine kinase. These data support the restoration of AMPAR activation via suppressing excessive PKC-mediated GRIP phosphorylation as a novel therapeutic approach to treat the neurobehavioral consequences of prenatal cocaine.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsCarrier ProteinsCentral Nervous System AgentsCocaineFemaleFrontal LobeGene ExpressionIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesLong-Term Synaptic DepressionMaleNerve Tissue ProteinsPhosphorylationPregnancyProtein Kinase CCarrier ProteinsCentral Nervous System AgentsCocaineGrip1 protein, ratIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsProtein Kinase CReceptors, AMPAsrc-Family Kinases

Identifiers

PMID19439608
PMCPMC2727739
OpenAlexW2052449365

What OpenQuestion holds

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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.