Evidence map›Paper›PMID 37624765›Full record

ArticlePloS one2023

Persistent extrasynaptic hyperdopaminergia in the mouse hippocampus induces plasticity and recognition memory deficits reversed by the atypical antipsychotic sulpiride.

Jill Rocchetti, Caroline Fasano, Gregory Dal-Bo, Elisa Guma, Salah El Mestikawy, Tak-Pan Wong, Gohar Fakhfouri, Bruno Giros

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

8 authors at 2 institutions in 2 countries.

Jill RocchettiDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.
Caroline FasanoDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.
Gregory Dal-BoDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.ORCID 0000-0001-7683-5854
Elisa GumaDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.
Salah El MestikawyDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.
Tak-Pan WongDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.ORCID 0000-0001-8611-4911
Gohar FakhfouriDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.
Bruno GirosDepartment of Psychiatry, Douglas Hospital, Mc Gill University, Montreal, Québec, Canada.ORCID 0000-0001-5876-9822
Douglas Mental Health University Institute · CACentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence suggests that subcortical hyperdopaminergia alters cognitive function in schizophrenia and antipsychotic drugs (APD) fail at rescuing cognitive deficits in patients. In a previous study, we showed that blocking D2 dopamine receptors (D2R), a core action of APD, led to profound reshaping of mesohippocampal fibers, deficits in synaptic transmission and impairments in learning and memory in the mouse hippocampus (HP). However, it is currently unknown how excessive dopamine affects HP-related cognitive functions, and how APD would impact HP functions in such a state. After verifying the presence of DAT-positive neuronal projections in the ventral (temporal), but not in the dorsal (septal), part of the HP, GBR12935, a blocker of dopamine transporter (DAT), was infused in the CA1 of adult C57Bl/6 mice to produce local hyperdopaminergia. Chronic GBR12935 infusion in temporal CA1 induced a mild learning impairment in the Morris Water Maze and abolished long-term recognition memory in novel-object (NORT) and object-place recognition tasks (OPRT). Deficits were accompanied by a significant decrease in DAT+ mesohippocampal fibers. Intrahippocampal or systemic treatment with sulpiride during GBR infusions improved the NORT deficit but not that of OPRT. In vitro application of GBR on hippocampal slices abolished long-term depression (LTD) of fEPSP in temporal CA1. LTD was rescued by co-application with sulpiride. In conclusion, chronic DAT blockade in temporal CA1 profoundly altered mesohippocampal modulation of hippocampal functions. Contrary to previous observations in normodopaminergic mice, antagonising D2Rs was beneficial for cognitive functions in the context of hippocampal hyperdopaminergia.

Indexed as

Antipsychotic AgentsAnimalsHippocampusMemory DisordersMiceMice, Inbred C57BLSulpirideAntipsychotic AgentsSulpiride

Identifiers

PMID37624765
PMCPMC10456148
OpenAlexW4386158646

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.