Evidence map›Paper›PMID 26162083›Full record

ArticlePloS one2015

Unique Effects of Acute Aripiprazole Treatment on the Dopamine D2 Receptor Downstream cAMP-PKA and Akt-GSK3β Signalling Pathways in Rats.

Bo Pan, Jiezhong Chen, Jiamei Lian, Xu-Feng Huang, Chao Deng

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Bo PanAntipsychotic Research Laboratory, Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia; Centre for Translational Neuroscience, School of Medicine, University of Wollongong, Wollongong, NSW, Australia.
Jiezhong ChenAntipsychotic Research Laboratory, Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia.
Jiamei LianAntipsychotic Research Laboratory, Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia; Centre for Translational Neuroscience, School of Medicine, University of Wollongong, Wollongong, NSW, Australia.
Xu-Feng HuangCentre for Translational Neuroscience, School of Medicine, University of Wollongong, Wollongong, NSW, Australia.
Chao DengAntipsychotic Research Laboratory, Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia; Centre for Translational Neuroscience, School of Medicine, University of Wollongong, Wollongong, NSW, Australia.
University of Wollongong · AUIllawarra Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aripiprazole is a wide-used antipsychotic drug with therapeutic effects on both positive and negative symptoms of schizophrenia, and reduced side-effects. Although aripiprazole was developed as a dopamine D2 receptor (D2R) partial agonist, all other D2R partial agonists that aimed to mimic aripiprazole failed to exert therapeutic effects in clinic. The present in vivo study aimed to investigate the effects of aripiprazole on the D2R downstream cAMP-PKA and Akt-GSK3β signalling pathways in comparison with a D2R antagonist--haloperidol and a D2R partial agonist--bifeprunox. Rats were injected once with aripiprazole (0.75 mg/kg, i.p.), bifeprunox (0.8 mg/kg, i.p.), haloperidol (0.1 mg/kg, i.p.) or vehicle. Five brain regions--the prefrontal cortex (PFC), nucleus accumbens (NAc), caudate putamen (CPu), ventral tegmental area (VTA) and substantia nigra (SN) were collected. The protein levels of PKA, Akt and GSK3β were measured by Western Blotting; the cAMP levels were examined by ELISA tests. The results showed that aripiprazole presented similar acute effects on PKA expression to haloperidol, but not bifeprunox, in the CPU and VTA. Additionally, aripiprazole was able to increase the phosphorylation of GSK3β in the PFC, NAc, CPu and SN, respectively, which cannot be achieved by bifeprunox and haloperidol. These results suggested that acute treatment of aripiprazole had differential effects on the cAMP-PKA and Akt-GSK3β signalling pathways from haloperidol and bifeprunox in these brain areas. This study further indicated that, by comparison with bifeprunox, the unique pharmacological profile of aripiprazole may be attributed to the relatively lower intrinsic activity at D2R.

Indexed as

AnimalsAripiprazoleBrainCyclic AMPCyclic AMP-Dependent Protein KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMalePhosphorylationProto-Oncogene Proteins c-aktRats, Sprague-DawleyReceptors, Dopamine D2Signal TransductionAripiprazoleCyclic AMPCyclic AMP-Dependent Protein KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratProto-Oncogene Proteins c-aktReceptors, Dopamine D2

Identifiers

PMID26162083
PMCPMC4498891
OpenAlexW787579729

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.