Evidence map›Paper›PMID 29481317›Full record

ArticleJournal of psychiatry & neuroscience : JPN2018

A postmortem analysis of NMDA ionotropic and group 1 metabotropic glutamate receptors in the nucleus accumbens in schizophrenia.

Jeremy S Lum, Samuel J Millard, Xu-Feng Huang, Lezanne Ooi, Kelly A Newell

Open access · hybridAbstract read
PubMed Full text at PMC
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Frontiers in pharmacology · 2018
    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

5 authors at 2 institutions in 1 country.

Jeremy S LumFrom the School of Medicine, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Newell); the Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Ooi, Newell); the Schizophrenia Research Institute, Darlinghurst, New South Wales, Australia (Lum); and the School of Biological Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Ooi).
Samuel J MillardFrom the School of Medicine, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Newell); the Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Ooi, Newell); the Schizophrenia Research Institute, Darlinghurst, New South Wales, Australia (Lum); and the School of Biological Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Ooi).
Xu-Feng HuangFrom the School of Medicine, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Newell); the Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Ooi, Newell); the Schizophrenia Research Institute, Darlinghurst, New South Wales, Australia (Lum); and the School of Biological Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Ooi).
Lezanne OoiFrom the School of Medicine, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Newell); the Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Ooi, Newell); the Schizophrenia Research Institute, Darlinghurst, New South Wales, Australia (Lum); and the School of Biological Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Ooi).
Kelly A NewellFrom the School of Medicine, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Newell); the Illawarra Health and Medical Research Institute, Wollongong, New South Wales, Australia (Lum, Millard, Huang, Ooi, Newell); the Schizophrenia Research Institute, Darlinghurst, New South Wales, Australia (Lum); and the School of Biological Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia (Ooi).
Schizophrenia Research Institute · AUIllawarra Health and Medical Research Institute · AU

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
BRAIN TISSUE RESOURCE CENTER FOR ALCOHOL RESEARCHR24AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI KRIL, JILLIAN JUNE · 2000 to 2011
$2.2M
NIAAA NIH HHS R24 AA012725NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

backgroundThe nucleus accumbens (NAcc) has been implicated in the pathology and treatment of schizophrenia. Recent postmortem evidence suggests a hyperglutamatergic state in the NAcc. With the present study we aimed to explore possible glutamatergic alterations in the NAcc of a large schizophrenia cohort.

methodsWe performed immunoblots on postmortem NAcc samples from 30 individuals who had schizophrenia and 30 matched controls. We examined the protein expression of primary glutamatergic receptors, including the

resultsProtein levels of glutamatergic receptors and endogenous regulators were not significantly different between the controls and individuals who had schizophrenia. Furthermore, mGluR5, but not mGluR1, showed a positive association with NMDA receptor subunits, suggesting differential interactions between these receptors in this brain region. LIMITATIONS: Investigation of these proteins in antipsychotic-naive individuals, in addition to the subregions of the NAcc and subcellular fractions, will strengthen future studies.

conclusionThe present study does not provide evidence for glutamatergic abnormalities within the NAcc of individuals with schizophrenia. Taken together with the results of previous studies, these findings suggest NMDA receptors and group 1 mGluRs are altered in a brain region-dependent manner in individuals with schizophrenia. The differential associations between mGluR1, mGluR5 and NMDA receptors observed in this study warrant further research into the interactions of these proteins and the implications for the therapeutic and adverse effect profile of glutamatergic-based novel therapeutics.

Indexed as

Case-Control StudiesFemaleHomer Scaffolding ProteinsHumansMaleMiddle AgedNerve Tissue ProteinsNucleus AccumbensReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateSchizophreniaHomer Scaffolding Proteinsmetabotropic glutamate receptor type 1Nerve Tissue ProteinsneurochondrinReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID29481317
PMCPMC5837882
OpenAlexW2794236424

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.