Evidence map›Paper›PMID 18641645›Full record

ArticleNature neuroscience2008

PICK1 uncoupling from mGluR7a causes absence-like seizures.

Federica Bertaso, Chuansheng Zhang, Astrid Scheschonka, Frédéric de Bock, Pierre Fontanaud, Philippe Marin, Richard L Huganir, Heinrich Betz, Joël Bockaert, Laurent Fagni and 1 more

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Overexpression of mGluMolecular neurobiology · 2025
    Article
  5. Article
  6. Pleiotropic Effects ofBiomolecules · 2025
    Review
  7. Review
  8. Review
  9. Modulation of Hippocampal Network Oscillation by PICK1-Dependent Cell Surface Expression of mGlu3 Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Phenotypic profiling of mGluGenes, brain, and behavior · 2020
    Article
  14. Article
  15. Biallelic GRM7 variants cause epilepsy, microcephaly, and cerebral atrophy.Annals of clinical and translational neurology · 2020
    Article
  16. Article
  17. Review
  18. Review
  19. Emerging Themes in PDZ Domain Signaling: Structure, Function, and Inhibition.International review of cell and molecular biology · 2019
    Review
  20. Metabotropic glutamate receptor trafficking.Molecular and cellular neurosciences · 2018
    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

11 authors at 5 institutions in 4 countries.

Federica BertasoCNRS UMR5203, Institut de Génomique Fonctionnelle, Montpellier, France, INSERM, U661, Montpellier, France and Université Montpellier, 1, 2, 141 rue de Cardonille, 34094 Montpellier, Cedex 5, France.
Chuansheng Zhang
Astrid Scheschonka
Frédéric de Bock
Pierre Fontanaud
Philippe Marin
Richard L Huganir
Heinrich Betz
Joël Bockaert
Laurent Fagni
Mireille Lerner-Natoli
Centre National de la Recherche Scientifique · FRInserm · FRMax Planck Society · DEHoward Hughes Medical Institute · USMax Planck Institute for Brain Research · DE

Funding

PDZ DOMAINS AND EXCITATORY SYNAPTIC FUNCTIONR01NS036715 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1997 to 2020
$8.6M
Howard Hughes Medical InstituteNINDS NIH HHS R01 NS036715
6 · The paper itself

Abstract

Absence epilepsy is a neurological disorder that causes a recurrent loss of consciousness and generalized spike-and-wave discharges on an electroencephalogram (EEG). The role of metabotropic glutamate receptors (mGluRs) and associated scaffolding proteins in absence epilepsy has been unclear to date. We investigated a possible role for these proteins in absence epilepsy, focusing on the mGluR7a receptor and its PDZ-interacting protein, protein interacting with C kinase 1 (PICK1), in rats and mice. Injection of a cell-permeant dominant-negative peptide or targeted mutation of the mGluR7a C terminus, both of which disrupt the interaction between the receptor and PDZ proteins, caused behavioral symptoms and EEG discharges that are characteristic of absence epilepsy. Inactivation of the Pick1 gene also facilitated pharmacological induction of the absence epilepsy phenotype. The cortex and thalamus, which are known to participate in absence epilepsy, were involved, but the hippocampus was not. Our results indicate that disruption of the mGluR7a-PICK1 complex is sufficient to induce absence epilepsy-like seizures in rats and mice, thus providing, to the best of our knowledge, the first animal model of metabotropic glutamate receptor-PDZ protein interaction in absence epilepsy.

Indexed as

Disease Models, AnimalAnimalsCarrier ProteinsCell Cycle ProteinsCells, CulturedElectrodes, ImplantedElectroencephalographyEpilepsy, AbsenceMaleMiceMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicNuclear ProteinsPeptidesPhenotypeCarrier ProteinsCell Cycle Proteinsmetabotropic glutamate receptor 7Nuclear ProteinsPeptidesPrkcabp protein, mouseProtein SubunitsReceptors, Metabotropic GlutamateRecombinant Fusion ProteinsTAT-R7-LV1 peptide

Identifiers

PMID18641645
PMCPMC2764992
OpenAlexW1994856122

What OpenQuestion holds

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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.