Evidence map›Paper›PMID 28094812›Full record

ArticleTranslational psychiatry2017

Putative presynaptic dopamine dysregulation in schizophrenia is supported by molecular evidence from post-mortem human midbrain.

T D Purves-Tyson, S J Owens, D A Rothmond, G M Halliday, K L Double, J Stevens, T McCrossin, C Shannon Weickert

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  12. Arrestin-3 Agonism at Dopamine DBiological psychiatry · 2023
    Article
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  14. Review
  15. Article
  16. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
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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

8 authors at 4 institutions in 1 country.

T D Purves-TysonSchizophrenia Research Institute, Sydney, NSW, Australia.
S J OwensSchizophrenia Research Institute, Sydney, NSW, Australia.
D A RothmondSchizophrenia Research Institute, Sydney, NSW, Australia.
G M HallidayAgeing and Neurodegeneration, Neuroscience Research Australia, Sydney, NSW, Australia.
K L DoubleDiscipline of Biomedical Science and Brain and Mind Centre, School of Medical Sciences, Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
J StevensSchizophrenia Research Institute, Sydney, NSW, Australia.
T McCrossinNew South Wales Brain Tissue Resource Centre, Discipline of Pathology, Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
C Shannon WeickertSchizophrenia Research Institute, Sydney, NSW, Australia.
University of Sydney · AUSchizophrenia Research Institute · AUUNSW Sydney · AUNeuroscience Research Australia · AU

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

The dopamine hypothesis of schizophrenia posits that increased subcortical dopamine underpins psychosis. In vivo imaging studies indicate an increased presynaptic dopamine synthesis capacity in striatal terminals and cell bodies in the midbrain in schizophrenia; however, measures of the dopamine-synthesising enzyme, tyrosine hydroxylase (TH), have not identified consistent changes. We hypothesise that dopamine dysregulation in schizophrenia could result from changes in expression of dopamine synthesis enzymes, receptors, transporters or catabolic enzymes. Gene expression of 12 dopamine-related molecules was examined in post-mortem midbrain (28 antipsychotic-treated schizophrenia cases/29 controls) using quantitative PCR. TH and the synaptic dopamine transporter (DAT) proteins were examined in post-mortem midbrain (26 antipsychotic-treated schizophrenia cases per 27 controls) using immunoblotting. TH and aromatic acid decarboxylase (AADC) mRNA and TH protein were unchanged in the midbrain in schizophrenia compared with controls. Dopamine receptor D2 short, vesicular monoamine transporter (VMAT2) and DAT mRNAs were significantly decreased in schizophrenia, with no change in DRD3 mRNA, DRD3nf mRNA and DAT protein between diagnostic groups. However, DAT protein was significantly increased in putatively treatment-resistant cases of schizophrenia compared to putatively treatment-responsive cases. Midbrain monoamine oxidase A (MAOA) mRNA was increased, whereas MAOB and catechol-O-methyl transferase mRNAs were unchanged in schizophrenia. We conclude that, whereas some mRNA changes are consistent with increased dopamine action (decreased DAT mRNA), others suggest reduced dopamine action (increased MAOA mRNA) in the midbrain in schizophrenia. Here, we identify a molecular signature of dopamine dysregulation in the midbrain in schizophrenia that mainly includes gene expression changes of molecules involved in dopamine synthesis and in regulating the time course of dopamine action.

Indexed as

AdultAgedAntipsychotic AgentsAutopsyBlotting, WesternCase-Control StudiesCatechol O-MethyltransferaseDopamineDopamine Plasma Membrane Transport ProteinsFemaleHumansMaleMesencephalonMiddle AgedMonoamine OxidaseNeostriatumAntipsychotic AgentsCatechol O-MethyltransferaseCOMT protein, humanDopamineDopamine Plasma Membrane Transport ProteinsDRD3 protein, humanMonoamine OxidaseReceptors, Dopamine D3RNA, MessengerSLC18A2 protein, humanTyrosine 3-MonooxygenaseVesicular Monoamine Transport Proteins

Identifiers

PMID28094812
PMCPMC5545725
OpenAlexW2578810188

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.