Evidence map›Paper›PMID 12363194›Full record

ReviewCellular and molecular neurobiology2002

Insights from mouse models of absence epilepsy into Ca2+ channel physiology and disease etiology.

Ricardo Felix

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Towards Zebrafish Models of CNS Channelopathies.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Animal models of epilepsy: use and limitations.Neuropsychiatric disease and treatment · 2014
    Review
  14. Regulation of high-voltage-activated CaWiley interdisciplinary reviews. Membrane transport and signaling · 2013
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Paroxysmal dyskinesias in mice.Movement disorders : official journal of the Movement Disorder Society · 2008
    Article
  20. Molecular targets for antiepileptic drug development.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2007
    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

1 author at 1 institution in 1 country.

Ricardo FelixDepartment of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies of the National Polytechnic Institute, Cinvestav-IPN, Mexico DF. rfelix@fisio.cinvestav.mx
Instituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Changes in intracellular Ca2+ ([Ca2+]i) levels provide signals that allow neurons to respond to a host of external stimuli. A major mechanism for elevating [Ca2+]i is the influx of extracellular Ca2+ through voltage-gated channels (Ca(V)) in the plasma membrane. Malfunction in Ca(V) due to mutations in genes encoding channel proteins are increasingly being implicated in causing disease conditions, termed channelopathies. 2. Seven spontaneous mutations with cerebellar ataxia and generalized absence epilepsy have been identified in mice (tottering, leaner, rolling Nagoya, rocker, lethargic, ducky, and stargazer), and these overlapping phenotypes are directly related to mutations in genes encoding the four separate subunits that together form the multimeric neuronal Ca(V) complex. 3. The discovery and systematic analysis of these animal models is helping to clarify how different mutations affect channel function and how altered channel function produces disease.

Indexed as

AnimalsBrainCalcium ChannelsCalcium SignalingCell MembraneCerebellar AtaxiaEpilepsy, AbsenceHumansMiceMice, Neurologic MutantsMutationNeuronsCalcium Channels

Identifiers

PMID12363194
PMCPMC11533750
OpenAlexW2159010791

What OpenQuestion holds

Textmetadata
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.