Evidence map›Paper›PMID 25989143›Full record

ArticleTranslational psychiatry2015

Altered functional brain network connectivity and glutamate system function in transgenic mice expressing truncated Disrupted-in-Schizophrenia 1.

N Dawson, M Kurihara, D M Thomson, C L Winchester, A McVie, J R Hedde, A D Randall, S Shen, P A Seymour, Z A Hughes and 5 more

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

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 38 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

15 authors at 5 institutions in 2 countries.

N Dawson1] Strathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde, Glasgow, UK [2] Centre for Neuroscience (CeNsUS), University of Strathclyde, Glasgow, UK [3] Psychiatric Research Institute for Neuroscience in Glasgow (PsyRING), Universities of Glasgow and Strathclyde, Glasgow, UK.
M KuriharaSchool of Physiology and Pharmacology, University of Bristol, Bristol, UK.
D M Thomson1] Psychiatric Research Institute for Neuroscience in Glasgow (PsyRING), Universities of Glasgow and Strathclyde, Glasgow, UK [2] Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
C L Winchester1] Strathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde, Glasgow, UK [2] Centre for Neuroscience (CeNsUS), University of Strathclyde, Glasgow, UK [3] Psychiatric Research Institute for Neuroscience in Glasgow (PsyRING), Universities of Glasgow and Strathclyde, Glasgow, UK.
A McVie1] Centre for Neuroscience (CeNsUS), University of Strathclyde, Glasgow, UK [2] Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
J R HeddePfizer Neuroscience Research Unit, Cambridge, MA, USA.
A D Randall1] School of Physiology and Pharmacology, University of Bristol, Bristol, UK [2] University of Exeter Medical School, University of Exeter, Hatherly Laboratories, Exeter, UK.
S Shen1] School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK [2] Regenerative Medicine Institute, School of Medicine, National University of Ireland, Galway, Ireland.
P A SeymourPfizer Neuroscience Research Unit, Cambridge, MA, USA.
Z A HughesPfizer Neuroscience Research Unit, Cambridge, MA, USA.
J DunlopPfizer Neuroscience Research Unit, Cambridge, MA, USA.
J T Brown1] School of Physiology and Pharmacology, University of Bristol, Bristol, UK [2] University of Exeter Medical School, University of Exeter, Hatherly Laboratories, Exeter, UK.
N J BrandonPfizer Neuroscience Research Unit, Cambridge, MA, USA.
B J Morris1] Psychiatric Research Institute for Neuroscience in Glasgow (PsyRING), Universities of Glasgow and Strathclyde, Glasgow, UK [2] Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
J A Pratt1] Strathclyde Institute of Pharmacy and Biomedical Science, University of Strathclyde, Glasgow, UK [2] Centre for Neuroscience (CeNsUS), University of Strathclyde, Glasgow, UK [3] Psychiatric Research Institute for Neuroscience in Glasgow (PsyRING), Universities of Glasgow and Strathclyde, Glasgow, UK.
Pfizer (United States) · USUniversity of Strathclyde · GBUniversity of Bristol · GBUniversity of Aberdeen · GBUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Considerable evidence implicates DISC1 as a susceptibility gene for multiple psychiatric diseases. DISC1 has been intensively studied at the molecular, cellular and behavioral level, but its role in regulating brain connectivity and brain network function remains unknown. Here, we utilize a set of complementary approaches to assess the functional brain network abnormalities present in mice expressing a truncated Disc1 gene (Disc1tr Hemi mice). Disc1tr Hemi mice exhibited hypometabolism in the prefrontal cortex (PFC) and reticular thalamus along with a reorganization of functional brain network connectivity that included compromised hippocampal-PFC connectivity. Altered hippocampal-PFC connectivity in Disc1tr Hemi mice was confirmed by electrophysiological analysis, with Disc1tr Hemi mice showing a reduced probability of presynaptic neurotransmitter release in the monosynaptic glutamatergic hippocampal CA1-PFC projection. Glutamate system dysfunction in Disc1tr Hemi mice was further supported by the attenuated cerebral metabolic response to the NMDA receptor (NMDAR) antagonist ketamine and decreased hippocampal expression of NMDAR subunits 2A and 2B in these animals. These data show that the Disc1 truncation in Disc1tr Hemi mice induces a range of translationally relevant endophenotypes underpinned by glutamate system dysfunction and altered brain connectivity.

Indexed as

AnimalsAutoradiographyBrainCA1 Region, HippocampalExcitatory Amino Acid AntagonistsGlutamic AcidHippocampusKetamineMiceMice, Inbred C57BLMice, TransgenicNerve Tissue ProteinsNeural PathwaysPatch-Clamp TechniquesPrefrontal CortexReceptors, N-Methyl-D-AspartateDisc1 protein, mouseExcitatory Amino Acid AntagonistsGlutamic AcidKetamineNerve Tissue ProteinsNR2B NMDA receptorReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25989143
PMCPMC4471291
OpenAlexW1497274479

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.