Evidence map›Paper›PMID 18479834›Full record

ArticleNeuroscience2008

Preferential relocation of the N-methyl-D-aspartate receptor NR1 subunit in nucleus accumbens neurons that contain dopamine D1 receptors in rats showing an apomorphine-induced sensorimotor gating deficit.

Y Hara, V M Pickel

Abstract read
In one paragraph

Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  8. Ventral striatal noradrenergic mechanisms contribute to sensorimotor gating deficits induced by amphetamine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    Article
  9. 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

2 authors at 1 institution in 1 country.

Y HaraDivision of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 East 69th Street KB-410, New York, NY 10021, USA.
V M Pickel
Cornell University · US

Funding

EM-TRANSMITTER INTERACTIONS OF STRIATAL OPIOID NEURONSR01DA004600 · NIDA · WEILL MEDICAL COLL OF CORNELL UNIV · PI PICKEL, VIRGINIA M · 1989 to 2013
$3.1M
ULTRASTRUCTURE OF MESOLIMBIC TRANSMITTER INTERACTIONSR37MH040342 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI PICKEL, VIRGINIA M · 1988 to 2007
$2.5M
ULTRASTRUCTURE OF MESOLIMBIC TRANSMITTER INTERACTIONSR01MH040342 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI PICKEL, VIRGINIA M · 1985 to 2012
$1.7M
NIDA NIH HHS DA04600NIDA NIH HHS R01 DA004600NIMH NIH HHS MH40342NIMH NIH HHS R01 MH040342NIMH NIH HHS R37 MH040342
6 · The paper itself

Abstract

Sensorimotor gating as measured by prepulse inhibition (PPI) to startle-evoking auditory stimulation (AS) is disrupted in schizophrenia and in rodents receiving systemic administration of apomorphine, a dopamine D1/D2 receptor agonist, or MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist. The functional analogies and our prior results showing apomorphine- and AS-induced relocation of the dopamine D1 receptor (D1R) in the nucleus accumbens (Acb) shell suggest that apomorphine and AS may affect the subcellular distribution of the NMDA receptor NR1 subunit, a protein that forms protein-protein interactions with the D1R. We quantitatively compared the electron microscopic immunogold labeling for NR1 in dendritic profiles distinguished with respect to presence of D1R immunoreactivity and location in the Acb shell or core of rats receiving a single s.c. injection of vehicle (VEH) or apomorphine (APO) alone, or combined with AS (VEH+AS, APO+AS). The rats in the APO+AS group were previously shown to have PPI deficits, whereas the rats in the VEH+AS group had normal PPI. A significantly higher percentage of plasmalemmal and a lower percentage of cytoplasmic NR1 immunogold particles were seen in D1R-labeled dendritic spines in the Acb shell of the APO+AS group compared with all other groups. D1R-containing small dendrites in the Acb shell of the APO+AS group also showed a significantly higher density of plasmalemmal and a lower density of cytoplasmic NR1 immunogold particles compared with VEH or APO groups. In the Acb core, the APO+AS group had significantly fewer dendritic spines co-expressing NR1 and D1R compared with VEH or VEH+AS groups. These results, together with our earlier findings, suggest that NMDA receptors are preferentially mobilized in D1R-containing Acb neurons of rats showing apomorphine-induced disruption of PPI in a paradigm using acoustic stimulation.

Indexed as

Acoustic StimulationAnimalsApomorphineImmunohistochemistryMaleMicroscopy, ElectronNeuronsNucleus AccumbensRatsRats, Sprague-DawleyReceptors, Dopamine D1Receptors, N-Methyl-D-AspartateReflex, StartleSubcellular FractionsApomorphineNR1A NMDA receptor, ratReceptors, Dopamine D1Receptors, N-Methyl-D-Aspartate

Identifiers

PMID18479834
PMCPMC2587121
OpenAlexW1983351987

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.