Evidence map›Paper›PMID 27382048›Full record

ArticleThe international journal of neuropsychopharmacology2016

Down-Regulation of Hippocampal Genes Regulating Dopaminergic, GABAergic, and Glutamatergic Function Following Combined Neonatal Phencyclidine and Post-Weaning Social Isolation of Rats as a Neurodevelopmental Model for Schizophrenia.

Philip Lr Gaskin, Maria Toledo-Rodriguez, Stephen Ph Alexander, Kevin Cf Fone

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-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

16 citing papers in PubMed, 41 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

4 authors at 2 institutions in 1 country.

Philip Lr GaskinSchool of Life Sciences, Medical School, Queen's Medical Centre, The University of Nottingham, United Kingdom (Drs Gaskin, Toledo-Rodriguez, Alexander, and Fone).
Maria Toledo-RodriguezSchool of Life Sciences, Medical School, Queen's Medical Centre, The University of Nottingham, United Kingdom (Drs Gaskin, Toledo-Rodriguez, Alexander, and Fone).
Stephen Ph AlexanderSchool of Life Sciences, Medical School, Queen's Medical Centre, The University of Nottingham, United Kingdom (Drs Gaskin, Toledo-Rodriguez, Alexander, and Fone).
Kevin Cf FoneSchool of Life Sciences, Medical School, Queen's Medical Centre, The University of Nottingham, United Kingdom (Drs Gaskin, Toledo-Rodriguez, Alexander, and Fone) kevin.fone@nottingham.ac.uk.
Queen's Medical Centre · GBUniversity of Nottingham · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

backgroundDysfunction of dopaminergic, GABAergic, and glutamatergic function underlies many core symptoms of schizophrenia. Combined neonatal injection of the N-methyl-D-aspartate (NMDA) receptor antagonist, phencyclidine (PCP), and post-weaning social isolation of rats produces a behavioral syndrome with translational relevance to several core symptoms of schizophrenia. This study uses DNA microarray to characterize alterations in hippocampal neurotransmitter-related gene expression and examines the ability of the sodium channel blocker, lamotrigine, to reverse behavioral changes in this model.

methodsFifty-four male Lister-hooded rat pups either received phencyclidine (PCP, 10mg/kg, s.c.) on post-natal days (PND) 7, 9, and 11 before being weaned on PND 23 into separate cages (isolation; PCP-SI; n = 31) or received vehicle injection and group-housing (2-4 per cage; V-GH; n = 23) from weaning. The effect of lamotrigine on locomotor activity, novel object recognition, and prepulse inhibition of acoustic startle was examined (PND 60-75) and drug-free hippocampal gene expression on PND 70.

resultsAcute lamotrigine (10-15mg/kg i.p.) reversed the hyperactivity and novel object recognition impairment induced by PCP-SI but had no effect on the prepulse inhibition deficit. Microarray revealed small but significant down-regulation of hippocampal genes involved in glutamate metabolism, dopamine neurotransmission, and GABA receptor signaling and in specific schizophrenia-linked genes, including parvalbumin (PVALB) and GAD67, in PCP-SI rats, which resemble changes reported in schizophrenia.

conclusionsFindings indicate that alterations in dopamine neurotransmission, glutamate metabolism, and GABA signaling may contribute to some of the behavioral deficits observed following PCP-SI, and that lamotrigine may have some utility as an adjunctive therapy to improve certain cognitive deficits symptoms in schizophrenia.

Indexed as

Behavior, AnimalPhencyclidineSchizophrenic PsychologySocial IsolationAnimalsAnimals, NewbornDisease Models, AnimalDopaminergic NeuronsGABAergic NeuronsGene Expression ProfilingGene Expression RegulationGenetic Predisposition to DiseaseGlutamic AcidHippocampusLamotrigineLocomotionGlutamic AcidLamotriginePhencyclidineSodium Channel BlockersTriazinesglutamateisolation rearinglamotriginemicroarrayphencyclidineschizophrenia

Identifiers

PMID27382048
PMCPMC5137279
OpenAlexW2470987720

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.