Evidence map›Paper›PMID 35677756›Full record

ArticleFrontiers in cellular neuroscience2022

Cannabinoid 1/2 Receptor Activation Induces Strain-Dependent Behavioral and Neurochemical Changes in Genetic Absence Epilepsy Rats From Strasbourg and Non-epileptic Control Rats.

Philippe De Deurwaerdère, Maurizio Casarrubea, Daniel Cassar, Manuela Radic, Emilie Puginier, Abdeslam Chagraoui, Giuseppe Crescimanno, Vincenzo Crunelli, Giuseppe Di Giovanni

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

9 authors at 5 institutions in 4 countries.

Philippe De DeurwaerdèreCentre National de la Recherche Scientifique, UMR 5287, Bordeaux Cedex, France.
Maurizio CasarrubeaLaboratory of Behavioral Physiology, Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), Human Physiology Section "Giuseppe Pagano", University of Palermo, Palermo, Italy.
Daniel CassarLaboratory of Neurophysiology, Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta, Msida, Malta.
Manuela RadicLaboratory of Neurophysiology, Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta, Msida, Malta.
Emilie PuginierCentre National de la Recherche Scientifique, UMR 5287, Bordeaux Cedex, France.
Abdeslam ChagraouiDepartment of Biomedical Sciences, Section of Neuroscience and Clinical Pharmacology, University of Cagliari, Cagliari, Italy.
Giuseppe CrescimannoLaboratory of Behavioral Physiology, Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), Human Physiology Section "Giuseppe Pagano", University of Palermo, Palermo, Italy.
Vincenzo CrunelliNeuroscience Division, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Giuseppe Di GiovanniLaboratory of Neurophysiology, Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, University of Malta, Msida, Malta.
University of Malta · MTCentre National de la Recherche Scientifique · FRUniversity of Palermo · ITCardiff University · GBInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Childhood absence epilepsy (CAE) is characterized by absence seizures, which are episodes of lack of consciousness accompanied by electrographic spike-wave discharges. About 60% of children and adolescents with absence seizures are affected by major neuropsychological comorbidities, including anxiety. Endocannabinoids and monoamines are likely involved in the pathophysiology of these CAE psychiatric comorbidities. Here, we show that the synthetic cannabinoid receptor type 1/2 (CB1/2R) agonist WIN 55,212-2 (2 mg/kg) has a strain-dependent effect on anxiety-like and motor behavior when assess in the hole board test and cerebral monoaminergic levels in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) and their non-epileptic control (NEC) rat strain. Using quantitative and Temporal pattern (T-pattern) analyses, we found that WIN 55,212-2 did not affect the emotional status of GAERS, but it was anxiolytic in NEC. Conversely, WIN 55,212-2 had a sedative effect in GAERS but was ineffective in NEC. Moreover, vehicle-treated GAERS more motivated to explore by implementing more complex and articulated strategies. These behavioral changes correlate with the reduction of 5-HT in the hippocampus and substantia nigra (SN) and noradrenaline (NA) in the entopeduncular nucleus (EPN) in vehicle-treated GAERS compared to NEC rats, which could contribute to their low anxiety status and hypermotility, respectively. On the other hand, the increased level of NA in the EPN and 5-HT in the SN is consistent with an activation of the basal ganglia output-mediated motor suppression observed in WIN 55,212-2-treated GAERS rats. These data support the view of a strain-dependent alteration of the endocannabinoid system in absence epilepsy by adding evidence of a lower emotional responsiveness and a basal ganglia hypersensitivity to cannabinoids in GAERS compared to NEC rats.

Indexed as

cannabinoid receptorsCB1CB2GABAglutamatehigh-pressure liquid chromatographystrain-dependent effectsthalamus

Identifiers

PMID35677756
PMCPMC9169225
OpenAlexW4281295102

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.