Evidence map›Paper›PMID 26365611›Full record

ArticleNeuroscience2015

Altered hippocampal plasticity by prenatal kynurenine administration, kynurenine-3-monoxygenase (KMO) deletion or galantamine.

C M Forrest, K McNair, M Pisar, O S Khalil, L G Darlington, T W Stone

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

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

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  12. Blockade of KAT II Facilitates LTP in Kynurenine 3-Monooxygenase Depleted Mice.International journal of tryptophan research : IJTR · 2021
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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

6 authors at 2 institutions in 1 country.

C M ForrestInstitute of Neuroscience and Psychology, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK.
K McNairInstitute of Neuroscience and Psychology, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK.
M PisarInstitute of Neuroscience and Psychology, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK.
O S KhalilInstitute of Neuroscience and Psychology, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK.
L G DarlingtonAshtead Hospital, The Warren, Ashtead, Surrey KT21 2SB, UK.
T W StoneInstitute of Neuroscience and Psychology, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK. Electronic address: Trevor.Stone@glasgow.ac.uk.
University of Glasgow · GBAshtead Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

Glutamate receptors sensitive to N-methyl-D-aspartate (NMDA) are involved in embryonic brain development but their activity may be modulated by the kynurenine pathway of tryptophan metabolism which includes an agonist (quinolinic acid) and an antagonist (kynurenic acid) at these receptors. Our previous work has shown that prenatal inhibition of the pathway produces abnormalities of brain development. In the present study kynurenine and probenecid (both 100mg/kg, doses known to increase kynurenic acid levels in the brain) were administered to female Wistar rats on embryonic days E14, E16 and E18 of gestation and the litter was allowed to develop to post-natal day P60. Western blotting revealed no changes in hippocampal expression of several proteins previously found to be altered by inhibition of the kynurenine pathway including the NMDA receptor subunits GluN1, GluN2A and GluN2B, as well as doublecortin, Proliferating Cell Nuclear Antigen (PCNA), sonic hedgehog and unco-ordinated (unc)-5H1 and 5H3. Mice lacking the enzyme kynurenine-3-monoxygenase (KMO) also showed no changes in hippocampal expression of several of these proteins or the 70-kDa and 100-kDa variants of Disrupted in Schizophrenia-1 (DISC1). Electrical excitability of pyramidal neurons in the CA1 region of hippocampal slices was unchanged, as was paired-pulse facilitation and inhibition. Long-term potentiation was decreased in the kynurenine-treated rats and in the KMO(-/-) mice, but galantamine reversed this effect in the presence of nicotinic receptor antagonists, consistent with evidence that it can potentiate glutamate at NMDA receptors. It is concluded that interference with the kynurenine pathway in utero can have lasting effects on brain function of the offspring, implying that the kynurenine pathway is involved in the regulation of early brain development.

Indexed as

Adjuvants, PharmaceuticAnimalsDoublecortin Domain ProteinsDoublecortin ProteinFemaleGalantamineGene Expression RegulationGestational AgeHippocampusIn Vitro TechniquesKynurenineKynurenine 3-MonooxygenaseLong-Term PotentiationMaleMiceMice, KnockoutAdjuvants, PharmaceuticDcx protein, ratDoublecortin Domain ProteinsDoublecortin ProteinGalantamineKynurenineKynurenine 3-MonooxygenaseMicrotubule-Associated ProteinsNeuropeptidesNootropic AgentsProbenecidReceptors, Glutamatekynurenic acidkynureninesneurodevelopmenttryptophan

Identifiers

PMID26365611
PMCPMC4642643
OpenAlexW1839855160

What OpenQuestion holds

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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.