Evidence map›Paper›PMID 9751781›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Targeted disruption of the Ca2+ channel beta3 subunit reduces N- and L-type Ca2+ channel activity and alters the voltage-dependent activation of P/Q-type Ca2+ channels in neurons.

Y Namkung, S M Smith, S B Lee, N V Skrypnyk, H L Kim, H Chin, R H Scheller, R W Tsien, H S Shin

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 95 citations in OpenAlex.

  1. Brain communications · 2026
    Article
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  5. Review
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  8. Blocking CaCell reports · 2018
    Article
  9. Article
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  11. Absence of plateau potentials in dLGN cells leads to a breakdown in retinogeniculate refinement.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  12. Article
  13. Article
  14. Regulation of high-voltage-activated CaWiley interdisciplinary reviews. Membrane transport and signaling · 2013
    Article
  15. Review
  16. Article
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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

9 authors at 1 institution in 1 country.

Y NamkungDepartment of Life Science, Pohang University of Science and Technology, San-31, Hyoja-Dong, Pohang, 790-784, Republic of Korea.
S M Smith
S B Lee
N V Skrypnyk
H L Kim
H Chin
R H Scheller
R W Tsien
H S Shin
Creative Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In comparison to the well characterized role of the principal subunit of voltage-gated Ca2+ channels, the pore-forming, antagonist-binding alpha1 subunit, considerably less is understood about how beta subunits contribute to neuronal Ca2+ channel function. We studied the role of the Ca2+ channel beta3 subunit, the major Ca2+ channel beta subunit in neurons, by using a gene-targeting strategy. The beta3 deficient (beta3-/-) animals were indistinguishable from the wild type (wt) with no gross morphological or histological differences. However, in sympathetic beta3-/- neurons, the L- and N-type current was significantly reduced relative to wt. Voltage-dependent activation of P/Q-type Ca2+ channels was described by two Boltzmann components with different voltage dependence, analogous to the "reluctant" and "willing" states reported for N-type channels. The absence of the beta3 subunit was associated with a hyperpolarizing shift of the "reluctant" component of activation. Norepinephrine inhibited wt and beta3-/- neurons similarly but the voltage sensitive component was greater for N-type than P/Q-type Ca2+ channels. The reduction in the expression of N-type Ca2+ channels in the beta3-/- mice may be expected to impair Ca2+ entry and therefore synaptic transmission in these animals. This effect may be reversed, at least in part, by the increase in the proportion of P/Q channels activated at less depolarized voltage levels.

Indexed as

AnimalsCalcium ChannelsFemaleIn Vitro TechniquesIon Channel GatingMaleMembrane PotentialsMiceMice, KnockoutNeuronsNorepinephrineProtein ConformationSynaptic TransmissionCalcium ChannelsNorepinephrine

Identifiers

PMID9751781
PMCPMC21756
OpenAlexW2090489014

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.