Evidence map›Paper›PMID 22076136›Full record

ArticlePloS one2011

Redistribution of CB1 cannabinoid receptors in the acute and chronic phases of pilocarpine-induced epilepsy.

Mária R Karlócai, Kinga Tóth, Masahiko Watanabe, Catherine Ledent, Gábor Juhász, Tamás F Freund, Zsófia Maglóczky

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.9field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  11. Circuit formation in the adult brain.The European journal of neuroscience · 2022
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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

7 authors at 5 institutions in 3 countries.

Mária R KarlócaiInstitute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary. karlocai.rita@koki.hu
Kinga Tóth
Masahiko Watanabe
Catherine Ledent
Gábor Juhász
Tamás F Freund
Zsófia Maglóczky
HUN-REN Institute of Experimental Medicine · HUEötvös Loránd University · HUHokkaido University · JPHungarian Academy of Sciences · HUUniversité Libre de Bruxelles · BE

Funding

ENDOGENOUS GABAERGIC ACTIVITY IN THE MAMMALIAN BRAINR01NS030549 · NINDS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MODY, ISTVAN · 1992 to 2018
$4.5M
Endogenous GABAergic ActivityR37NS030549 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODY, ISTVAN · 2001 to 2007
$2.7M
NINDS NIH HHS R01 NS030549NINDS NIH HHS R37 NS030549
6 · The paper itself

Abstract

The endocannabinoid system plays a central role in retrograde synaptic communication and may control the spread of activity in an epileptic network. Using the pilocarpine model of temporal lobe epilepsy we examined the expression pattern of the Type 1 cannabinoid receptor (CB1-R) in the hippocampi of CD1 mice at survival times of 2 hours, 1 day, 3 days and 2 months (acute, latent and chronic phases). Based on the behavioral signs of the acute seizures, animals were classified as "weakly" or "strongly" epileptic using the modified Racine scale. Mice of the weak group had mild seizures, whereas seizures in the strong group were frequent with intense motor symptoms and the majority of these animals developed sclerosis in the chronic phase. In control samples the most intense staining of CB1-R-positive fibers was found in the molecular layer of the dentate gyrus and in str. pyramidale of the cornu Ammonis. In weak animals no significant changes were seen at any survival time compared to controls. In strong animals, however, in the acute phase, a massive reduction in CB1-R-stained terminals occurred in the hippocampus. In the latent phase CB1-R immunoreactivity gradually recovered. In the chronic phase, CB1-immunostaining in sclerotic samples was stronger throughout the hippocampus. Quantitative electron microscopic analysis showed an increase in the number of CB1-R-positive terminals in the dentate gyrus. Moreover, the number of immunogold particles significantly increased in GABAergic terminals. Our results suggest a proconvulsive downregulation of CB1 receptors in the acute phase most probably due to receptor internalization, followed by compensatory upregulation and sprouting in the chronic phase of epilepsy. In conclusion, the changes in CB1 receptor expression pattern revealed in this study are associated with the severity of hippocampal injury initiated by acute seizures that ultimately leads to sclerosis in the vulnerable regions in the chronic phase.

Indexed as

Acute DiseaseAnimalsChronic DiseaseElectrophysiologyEpilepsy, Temporal LobeHippocampusImmunoenzyme TechniquesMaleMiceMice, KnockoutMuscarinic AgonistsNeuronsPilocarpineReceptor, Cannabinoid, CB1Survival RateMuscarinic AgonistsPilocarpineReceptor, Cannabinoid, CB1

Identifiers

PMID22076136
PMCPMC3208595
OpenAlexW1985249962

What OpenQuestion holds

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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.