Evidence map›Paper›PMID 10864934›Full record

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

Alternative splicing in the cytoplasmic II-III loop of the N-type Ca channel alpha 1B subunit: functional differences are beta subunit-specific.

J Q Pan, D Lipscombe

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 67 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2026
    Article
  2. Mechanism of gabapentinoid potentiation of opioid effects on cyclic AMP signaling in neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. The CaScientific reports · 2018
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Differential role of N-type calcium channel splice isoforms in pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  14. Article
  15. Article
  16. Developmentally regulated actions of alcohol on hippocampal glutamatergic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  17. Cumulative inactivation of N-type CaV2.2 calcium channels modified by alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  18. Review
  19. Review
  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

2 authors at 1 institution in 1 country.

J Q PanDepartment of Neuroscience, Brown University, Providence, Rhode Island 02912, USA.
D Lipscombe
Brown University · US

Funding

NEURONAL CALCIUM CHANNELS--REGULATION AND FUNCTIONR01NS029967 · NINDS · BROWN UNIVERSITY · PI LIPSCOMBE, DIANE · 1997 to 2009
$3.0M
NEURONAL CALIUM CHANNELS--REGULATION AND FUNCTIONR29NS029967 · NINDS · BROWN UNIVERSITY · PI LIPSCOMBE, DIANE · 1992 to 1996
–
NINDS NIH HHS NS01927NINDS NIH HHS NS29967NINDS NIH HHS R01 NS029967
6 · The paper itself

Abstract

Structural diversity of voltage-gated Ca channels underlies much of the functional diversity in Ca signaling in neurons. Alternative splicing is an important mechanism for generating structural variants within a single gene family. In this paper, we show the expression pattern of an alternatively spliced 21 amino acid encoding exon in the II-III cytoplasmic loop region of the N-type Ca channel alpha(1B) subunit and assess its functional impact. Exon-containing alpha(1B) mRNA dominated in sympathetic ganglia and was present in approximately 50% of alpha(1B) mRNA in spinal cord and caudal regions of the brain and in the minority of alpha(1B) mRNA in neocortex, hippocampus, and cerebellum (<20%). The II-III loop exon affected voltage-dependent inactivation of the N-type Ca channel. Steady-state inactivation curves were shifted to more depolarized potentials without affects on either the rate or voltage dependence of channel opening. Differences in voltage-dependent inactivation between alpha(1B) splice variants were most clearly manifested in the presence of Ca channel beta(1b) or beta(4), rather than beta(2a) or beta(3), subunits. Our results suggest that exon-lacking alpha(1B) splice variants that associate with beta(1b) and beta(4) subunits will be susceptible to voltage-dependent inactivation at voltages in the range of neuronal resting membrane potentials (-60 to -80 mV). In contrast, alpha(1B) splice variants that associate with either beta(2a) or beta(3) subunits will be relatively resistant to inactivation at these voltages. The potential to mix and match multiple alpha(1B) splice variants and beta subunits probably represents a mechanism for controlling the plasticity of excitation-secretion coupling at different synapses.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsBrainCalcium Channels, N-TypeCerebellumExonsFemaleGanglia, SympatheticGenetic VariationHippocampusLiverMacromolecular SubstancesMembrane PotentialsMolecular Sequence DataNeocortexCalcium Channels, N-TypeMacromolecular SubstancesRecombinant Proteins

Identifiers

PMID10864934
PMCPMC6772276
OpenAlexW2096395994

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.