Evidence map›Paper›PMID 10908603›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Reduced voltage sensitivity of activation of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation rolling Nagoya (tg(rol)).

Y Mori, M Wakamori, S Oda, C F Fletcher, N Sekiguchi, E Mori, N G Copeland, N A Jenkins, K Matsushita, Z Matsuyama and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.9field-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

52 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Rare CACNA1A mutations leading to congenital ataxia.Pflugers Archiv : European journal of physiology · 2020
    Review
  7. Review
  8. A mutation in CaThe Journal of general physiology · 2019
    Article
  9. Article
  10. Article
  11. The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016
    Review
  12. Article
  13. Article
  14. Piebald mutation on a C57BL/6J background.The Journal of veterinary medical science · 2015
    Article
  15. Article
  16. Article
  17. Rolling Nagoya mouse strain (PROD-rol/rol) with classic piebald mutation.The Journal of veterinary medical science · 2014
    Article
  18. GABABiology and medicine (Aligarh) · 2014
    Article
  19. Cerebellar ataxia by enhanced Ca(V)2.1 currents is alleviated by Ca2+-dependent K+-channel activators in Cacna1a(S218L) mutant mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  20. 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

11 authors at 5 institutions in 2 countries.

Y MoriDepartment of Information Physiology, National Institute for Physiological Sciences, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan. moriy@nips.ac.jp
M Wakamori
S Oda
C F Fletcher
N Sekiguchi
E Mori
N G Copeland
N A Jenkins
K Matsushita
Z Matsuyama
K Imoto
National Institute for Physiological Sciences · JPBioScience Laboratories (United States) · USThe Graduate University for Advanced Studies, SOKENDAI · JPNagoya University · JPNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent genetic analyses have revealed an important association of the gene encoding the P/Q-type voltage-dependent Ca(2+) channel alpha(1A) subunit with hereditary neurological disorders. We have identified the ataxic mouse mutation, rolling Nagoya (tg(rol)), in the alpha(1A) gene that leads to a charge-neutralizing arginine-to-glycine substitution at position 1262 in the voltage sensor-forming segment S4 in repeat III. Ca(2+) channel currents in acutely dissociated Purkinje cells, where P-type is the dominant type, showed a marked decrease in slope and a depolarizing shift by 8 mV of the conductance-voltage curve and reduction in current density in tg(rol) mouse cerebella, compared with those in wild-type. Compatible functional change was induced by the tg(rol) mutation in the recombinant alpha(1A) channel, indicating that a defect in voltage sensor of P/Q-type Ca(2+) channels is the direct consequence of the tg(rol) mutation. Furthermore, somatic whole-cell recording of mutant Purkinje cells displayed only abortive Na(+) burst activity and hardly exhibited Ca(2+) spike activity in cerebellar slices. Thus, in tg(rol) mice, reduced voltage sensitivity, which may derive from a gating charge defect, and diminished activity of the P-type alpha(1A) Ca(2+) channel significantly impair integrative properties of Purkinje neurons, presumably resulting in locomotor deficits.

Indexed as

Action PotentialsAllelesAmino Acid SubstitutionAnimalsAtaxiaCalcium Channels, N-TypeElectric StimulationElectrophysiologyFemaleIon Channel GatingMaleMiceMice, CongenicMice, Inbred C3HMice, Neurologic MutantsPhenotypeCalcium Channels, N-TypeRecombinant Proteins

Identifiers

PMID10908603
PMCPMC6772543
OpenAlexW1630474277

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.