Evidence map›Paper›PMID 8255738›Full record

ArticlePflugers Archiv : European journal of physiology1993

Phosphorylation enhances inactivation of N-type calcium channel current in bullfrog sympathetic neurons.

M A Werz, K S Elmslie, S W Jones

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Calcium channels: unanswered questions.Journal of bioenergetics and biomembranes · 2003
    Review
  5. Article
  6. Reluctant gating of single N-type calcium channels during neurotransmitter-induced inhibition in bullfrog sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  7. kappa- and mu-opioids reverse the somatostatin inhibition of Ca2+ currents in ciliary and dorsal root ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    Article
  8. Article
  9. Article
  10. Oxidation regulates cloned neuronal voltage-dependent Ca2+ channels expressed in Xenopus oocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  11. Overview of voltage-dependent calcium channels.Journal of bioenergetics and biomembranes · 1998
    Review
  12. Article
  13. Article
  14. Identification of the single channels that underlie the N-type and L-type calcium currents in bullfrog sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    Article
  15. Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

M A WerzDepartment of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106.
K S Elmslie
S W Jones
Case Western Reserve University · US

Funding

Translational Training Program in Pulmonary Biology and MedicineT32HL007563 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Melanie Koenigshoff · 1985 to 2026
$12.3M
PEPTIDE ACTION IN AUTONOMIC GANGLIAR01NS024471 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI JONES, STEPHEN W · 1986 to 2007
$2.0M
NHLBI NIH HHS HL 07563NINDS NIH HHS NS 08528NINDS NIH HHS NS 24471
6 · The paper itself

Abstract

We have investigated the effects of phosphatase and protein kinase inhibitors on calcium channel currents of bullfrog sympathetic neurons using the whole cell configuration of the patch clamp technique. Intracellular dialysis with the phosphatase inhibitors okadaic acid and calyculin A markedly enhanced the decline of inward current during a depolarizing voltage step. Tail current analysis demonstrated that this was genuine inactivation of calcium channel current, not activation of an outward current. The rapidly inactivating current is N-type calcium current (blocked by omega-conotoxin and resistant to nifedipine). Staurosporine, a nonselective protein kinase inhibitor, prevented the action of okadaic acid, suggesting that protein phosphorylation is involved. Under control conditions, the time course of inactivation could be described by the sum of two exponentials (tau = 150 ms and 1200 ms), plus a constant (apparently noninactivating) component, during depolarizations lasting 2 s. Okadaic acid induced a rapid inactivation process (tau = 15 ms) that was absent or negligible under control conditions, without obvious effect on the two slower time constants. As in control cells, inactivation in okadaic-acid-treated cells was strongest near -20 mV, with less inactivation at more positive voltages. However, inactivation did not depend on calcium influx. Modulation of calcium channel activity by phosphorylation may underly the spontaneous shift between inactivating and noninactivating modes recently observed for N-type calcium channels. Differences in basal phosphorylation levels could also explain why N-type calcium channels, originally described as rapidly and completely inactivating, inactivate slowly and incompletely in many neurons.

Indexed as

AnimalsCalcium Channel BlockersCalcium ChannelsEthers, CyclicNeuronsOkadaic AcidPhosphoric Monoester HydrolasesPhosphorylationProtein Kinase InhibitorsProtein KinasesRana catesbeianaSympathetic Nervous SystemCalcium Channel BlockersCalcium ChannelsEthers, CyclicOkadaic AcidPhosphoric Monoester HydrolasesProtein Kinase InhibitorsProtein Kinases

Identifiers

PMID8255738
OpenAlexW2077176434

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.