Evidence map›Paper›PMID 35370690›Full record

ArticleFrontiers in pharmacology2022

Acute Ketamine Facilitates Fear Memory Extinction in a Rat Model of PTSD Along With Restoring Glutamatergic Alterations and Dendritic Atrophy in the Prefrontal Cortex.

Nathalie Sala, Caterina Paoli, Tiziana Bonifacino, Jessica Mingardi, Emanuele Schiavon, Luca La Via, Marco Milanese, Paolo Tornese, Ashok K Datusalia, Jessica Rosa and 10 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 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

20 authors at 7 institutions in 3 countries.

Nathalie SalaLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Caterina PaoliLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Tiziana BonifacinoDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, Genoa, Italy.
Jessica MingardiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Emanuele SchiavonDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Luca La ViaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Marco MilaneseDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, Genoa, Italy.
Paolo TorneseLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Ashok K DatusaliaLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Jessica RosaLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Roberta FacchinettiDepartment of Physiology and Pharmacology "Vittorio Erspamer", SAPIENZA University of Rome, Rome, Italy.
Giulia FrumentoDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, Genoa, Italy.
Giulia CariniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Floramarida Salerno ScarzellaDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Caterina ScuderiDepartment of Physiology and Pharmacology "Vittorio Erspamer", SAPIENZA University of Rome, Rome, Italy.
Lia FortiDepartment of Biotechnology and Life Sciences, University of Insubria, Busto Arsizio, Italy.
Alessandro BarbonDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Giambattista BonannoDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, Genoa, Italy.
Maurizio PopoliLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università Degli Studi di Milano, Milano, Italy.
Laura MusazziSchool of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
University of Milan · ITUniversity of Brescia · ITUniversity of Genoa · ITUniversity of Insubria · ITSapienza University of Rome · ITUniversity of Milano-Bicocca · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress represents a major risk factor for psychiatric disorders, including post-traumatic stress disorder (PTSD). Recently, we dissected the destabilizing effects of acute stress on the excitatory glutamate system in the prefrontal cortex (PFC). Here, we assessed the effects of single subanesthetic administration of ketamine (10 mg/kg) on glutamate transmission and dendritic arborization in the PFC of footshock (FS)-stressed rats, along with changes in depressive, anxious, and fear extinction behaviors. We found that ketamine, while inducing a mild increase of glutamate release in the PFC of naïve rats, blocked the acute stress-induced enhancement of glutamate release when administered 24 or 72 h before or 6 h after FS. Accordingly, the treatment with ketamine 6 h after FS also reduced the stress-dependent increase of spontaneous excitatory postsynaptic current (sEPSC) amplitude in prelimbic (PL)-PFC. At the same time, ketamine injection 6 h after FS was found to rescue apical dendritic retraction of pyramidal neurons induced by acute stress in PL-PFC and facilitated contextual fear extinction. These results show rapid effects of ketamine in animals subjected to acute FS, in line with previous studies suggesting a therapeutic action of the drug in PTSD models. Our data are consistent with a mechanism of ketamine involving re-establishment of synaptic homeostasis, through restoration of glutamate release, and structural remodeling of dendrites.

Indexed as

acute stressanimal modeldendritic arborizationfear extinctionglutamate transmissionketamineprefrontal cortex (PFC)PTSD

Identifiers

PMID35370690
PMCPMC8968915
OpenAlexW4220821679

What OpenQuestion holds

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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.