Evidence map›Paper›PMID 39242923›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2024

Multi-level therapeutic actions of cannabidiol in ketamine-induced schizophrenia psychopathology in male rats.

Charalampos Brakatselos, Alexia Polissidis, George Ntoulas, Michail-Zois Asprogerakas, Olga Tsarna, Anastasia Vamvaka-Iakovou, Gerasimos Nakas, Anastasios Delis, Petros Tzimas, Leandros Skaltsounis and 5 more

Abstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Charalampos BrakatselosDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.ORCID 0009-0007-4889-2633
Alexia PolissidisCenter of Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, 11527, Athens, Greece.
George NtoulasDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.
Michail-Zois AsprogerakasDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.
Olga TsarnaDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.
Anastasia Vamvaka-IakovouInstitute of Biosciences & Applications, NCSR Demokritos, Athens, Greece.
Gerasimos NakasDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.
Anastasios DelisCenter of Basic Research, Biological Imaging Unit, Biomedical Research Foundation Academy of Athens, 11527, Athens, Greece.
Petros TzimasDepartment of Pharmacognosy and Natural Product Chemistry, Faculty of Pharmacy, National and Kapodistrian University of Athens, 15771, Athens, Greece.
Leandros SkaltsounisDepartment of Pharmacognosy and Natural Product Chemistry, Faculty of Pharmacy, National and Kapodistrian University of Athens, 15771, Athens, Greece.
Joana SilvaLife and Health Sciences Research Institute (ICVS), University of Minho, Braga, Portugal.
Foteini DelisDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece.
Joao Filipe OliveiraLife and Health Sciences Research Institute (ICVS), University of Minho, Braga, Portugal.ORCID 0000-0002-1005-2328
Ioannis SotiropoulosInstitute of Biosciences & Applications, NCSR Demokritos, Athens, Greece.
Katerina AntoniouDepartment of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110, Ioannina, Greece. kantoniou@uoi.gr.ORCID 0000-0002-2876-207X

Funding

Uncovering stress-induced mechanisms of Tau pathology in Alzheimer's diseaseRF1AG069941 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Clarissa Leigh Waites · 2020 to 2026
$5.5M
General Secretariat for Research and Technology (GSRT) 02075General Secretariat for Research and Technology (GSRT) 04301General Secretariat for Research and Technology (GSRT) 1203"la Caixa" Foundation (Caixa Foundation) 15493"la Caixa" Foundation (Caixa Foundation) 52410024NIA NIH HHS RF1 AG069941
6 · The paper itself

Abstract

Repeated administration of ketamine (KET) has been used to model schizophrenia-like symptomatology in rodents, but the psychotomimetic neurobiological and neuroanatomical underpinnings remain elusive. In parallel, the unmet need for a better treatment of schizophrenia requires the development of novel therapeutic strategies. Cannabidiol (CBD), a major non-addictive phytocannabinoid has been linked to antipsychotic effects with unclear mechanistic basis. Therefore, this study aims to clarify the neurobiological substrate of repeated KET administration model and to evaluate CBD's antipsychotic potential and neurobiological basis. CBD-treated male rats with and without prior repeated KET administration underwent behavioral analyses, followed by multilevel analysis of different brain areas including dopaminergic and glutamatergic activity, synaptic signaling, as well as electrophysiological recordings for the assessment of corticohippocampal and corticostriatal network activity. Repeated KET model is characterized by schizophrenia-like symptomatology and alterations in glutamatergic and dopaminergic activity mainly in the PFC and the dorsomedial striatum (DMS), through a bi-directional pattern. These observations are accompanied by glutamatergic/GABAergic deviations paralleled to impaired function of parvalbumin- and cholecystokinin-positive interneurons, indicative of excitation/inhibition (E/I) imbalance. Moreover, CBD counteracted the schizophrenia-like behavioral phenotype as well as reverted prefrontal abnormalities and ventral hippocampal E/I deficits, while partially modulated dorsostriatal dysregulations. This study adds novel insights to our understanding of the KET-induced schizophrenia-related brain pathology, as well as the CBD antipsychotic action through a region-specific set of modulations in the corticohippocampal and costicostrtiatal circuitry of KET-induced profile contributing to the development of novel therapeutic strategies focused on the ECS and E/I imbalance restoration.

Indexed as

Antipsychotic AgentsCannabidiolKetamineSchizophreniaAnimalsBrainDisease Models, AnimalMaleRatsRats, Sprague-DawleyAntipsychotic AgentsCannabidiolKetamine

Identifiers

PMID39242923
PMCPMC11631973

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.