Evidence map›Paper›PMID 8817381›Full record

ArticleThe Journal of general physiology1996

L-type Ca2+ channels access multiple open states to produce two components of Bay K 8644-dependent current in GH3 cells.

D M Fass, E S Levitan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. CaChannels (Austin, Tex.) · 2020
    Review
  2. Article
  3. Article
  4. Gating of the HypoPP-1 mutations: I. Mutant-specific effects and cooperativity.Pflugers Archiv : European journal of physiology · 2007
    Article
  5. Article
  6. Article
  7. Tonic dopamine inhibition of L-type Ca2+ channel activity reduces alpha1D Ca2+ channel gene expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    Article
  8. Article
  9. Modulation of the cloned skeletal muscle L-type Ca2+ channel by anchored cAMP-dependent protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    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.

D M FassDepartment of Neuroscience, University of Pittsburgh, Pennsylvania 15261, USA.
E S Levitan
University of Pittsburgh · US

Funding

Dense-Core Vesicle Circulation, Capture and Synaptic Neuropeptide ReleaseR01NS032385 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI EDWIN S LEVITAN · 1995 to 2026
$13.0M
REGULATION OF PITUITARY ION CHANNELSR29NS029804 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEVITAN, EDWIN S · 1991 to 1995
–
NIMH NIH HHS MH18273NINDS NIH HHS NS29804NINDS NIH HHS NS32385
6 · The paper itself

Abstract

To determine the number of L-channel populations responsible for producing the two components of whole-cell L-type Ca2+ channel current revealed by Bay K 8644 (Fass, D.M., and E.S. Levitan. 1996. J. Gen. Physiol. 108:1-11), L-type Ca2+ channel activity was recorded in cell-attached patches. Ensemble tail currents from most (six out of nine) single-channel patches had double-exponential time courses, with time constants that were similar to whole-cell tail current decay values. Also, in single-channel patches subjected to two different levels of depolarization, ensemble tail currents exactly reproduced the voltage dependence of activation of the two whole-cell components: The slow component is activated at more negative potentials than the fast component. In addition, deactivation of Bay K 8644-modified whole-cell L-current was slower after long (100-ms) depolarizations than after short (20-ms) depolarizations, and this phenomenon was also evident in ensemble tail currents from single L-channels. Thus, a single population of L-channels can produce the two components of macroscopic L-current deactivation. To determine how individual L-channels produce multiple macroscopic tail current components, we constructed ensemble tail currents from traces that contained a single opening upon repolarization and no reopenings. These ensemble tails were biexponential. This type of analysis also revealed that reopenings do not contribute to the slowing of tail current deactivation after long depolarizations. Thus, individual L-channels must have access to several open states to produce multiple macroscopic current components. We also obtained evidence that access to these open states can vary over time. Use of several open states may give L-channels the flexibility to participate in many cell functions.

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAnimalsCalcium ChannelsCells, CulturedMembrane PotentialsPituitary GlandRats3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterCalcium Channels

Identifiers

PMID8817381
PMCPMC2229299
OpenAlexW2138044745

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.