Evidence map›Paper›PMID 28154892›Full record

ArticlePsychopharmacology2017

Differential effects of antipsychotic and propsychotic drugs on prepulse inhibition and locomotor activity in Roman high- (RHA) and low-avoidance (RLA) rats.

Ignasi Oliveras, Ana Sánchez-González, Daniel Sampedro-Viana, Maria Antonietta Piludu, Cristóbal Río-Alamos, Osvaldo Giorgi, Maria G Corda, Susana Aznar, Javier González-Maeso, Cristina Gerbolés and 4 more

Open access · greenAbstract read
In one paragraph

Article in Psychopharmacology, 2017. 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
0.6field-weighted citation impact, top 40% 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, 18 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

14 authors at 4 institutions in 4 countries.

Ignasi OliverasDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Ana Sánchez-GonzálezDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Daniel Sampedro-VianaDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Maria Antonietta PiluduDepartment of Life and Environmental Sciences, Section of Pharmaceutical, Pharmacological and Nutraceutical Sciences, University of Cagliari, 09124, Cagliari, Italy.
Cristóbal Río-AlamosDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Osvaldo GiorgiDepartment of Life and Environmental Sciences, Section of Pharmaceutical, Pharmacological and Nutraceutical Sciences, University of Cagliari, 09124, Cagliari, Italy.
Maria G CordaDepartment of Life and Environmental Sciences, Section of Pharmaceutical, Pharmacological and Nutraceutical Sciences, University of Cagliari, 09124, Cagliari, Italy.
Susana AznarResearch Laboratory for Stereology and Neuroscience, Bispebjerg and Frederiksberg Hospitals, Copenhagen, Denmark.
Javier González-MaesoDepartment of Physiology and Biophysics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, 23298, USA.
Cristina GerbolésDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Gloria BlázquezDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Toni CañeteDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Adolf TobeñaDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Alberto Fernández-TeruelDepartment of Psychiatry and Forensic Medicine, Institute of Neurosciences, Universidad Autónoma de Barcelona, 08193 Bellaterra, Barcelona, Spain. albert.fernandez.teruel@uab.cat.
Universitat Autònoma de Barcelona · ESUniversity of Cagliari · ITFrederiksberg Hospital · DKVirginia Commonwealth University · US

Funding

Structure and function of the 5HT2A/mGluR2 complex in schizophreniaR01MH084894 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI Javier Gonzalez-Maeso · 2009 to 2026
$6.8M
Preclinical role of HDAC2 in mGlu2-dependent schizophrenia treatmentR01MH111940 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI GONZÁLEZ-MAESO, JAVIER · 2017 to 2021
$1.5M
NIMH NIH HHS R01 MH084894NIMH NIH HHS R01 MH111940
6 · The paper itself

Abstract

rationaleAnimal models with predictive and construct validity are necessary for developing novel and efficient therapeutics for psychiatric disorders.

objectivesWe have carried out a pharmacological characterization of the Roman high- (RHA-I) and low-avoidance (RLA-I) rat strains with different acutely administered propsychotic (DOI, MK-801) and antipsychotic drugs (haloperidol, clozapine), as well as apomorphine, on prepulse inhibition (PPI) of startle and locomotor activity (activity cages).

resultsRHA-I rats display a consistent deficit of PPI compared with RLA-I rats. The typical antipsychotic haloperidol (dopamine D2 receptor antagonist) reversed the PPI deficit characteristic of RHA-I rats (in particular at 65 and 70 dB prepulse intensities) and reduced locomotion in both strains. The atypical antipsychotic clozapine (serotonin/dopamine receptor antagonist) did not affect PPI in either strain, but decreased locomotion in a dose-dependent manner in both rat strains. The mixed dopamine D1/D2 agonist, apomorphine, at the dose of 0.05 mg/kg, decreased PPI in RHA-I, but not RLA-I rats. The hallucinogen drug DOI (5-HT2A agonist; 0.1-1.0 mg/kg) disrupted PPI in RLA-I rats in a dose-dependent manner at the 70 dB prepulse intensity, while in RHA-I rats, only the 0.5 mg/kg dose impaired PPI at the 80 dB prepulse intensity. DOI slightly decreased locomotion in both strains. Finally, clozapine attenuated the PPI impairment induced by the NMDA receptor antagonist MK-801 only in RLA-I rats.

conclusionsThese results add experimental evidence to the view that RHA-I rats represent a model with predictive and construct validity of some dopamine and 5-HT2A receptor-related features of schizophrenia.

Indexed as

AmphetaminesAnimalsAntipsychotic AgentsApomorphineAvoidance LearningClozapineDizocilpine MaleateDopamine AgonistsDopamine AntagonistsExcitatory Amino Acid AntagonistsHaloperidolLocomotionMalePrepulse InhibitionRatsReceptor, Serotonin, 5-HT2A4-iodo-2,5-dimethoxyphenylisopropylamineAmphetaminesAntipsychotic AgentsApomorphineClozapineDizocilpine MaleateDopamine AgonistsDopamine AntagonistsExcitatory Amino Acid AntagonistsHaloperidolReceptor, Serotonin, 5-HT2ASerotonin 5-HT2 Receptor AgonistsSerotonin AntagonistsActivityAntipsychotic drugsGenetically based rat modelPredictive validityPrepulse inhibitionPropsychotic drugsRoman high- and low-avoidance ratsSchizophrenia

Identifiers

PMID28154892
PMCPMC5492384
OpenAlexW2583963876

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Registered trials

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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.