Evidence map›Paper›PMID 1656456›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1991

Tonic inhibition and rebound facilitation of a neuronal calcium channel by a GTP-binding protein.

H Kasai

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Syntaxin 1A supports voltage-dependent inhibition of alpha1B Ca2+ channels by Gbetagamma in chick sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
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  9. The Ca2+ channel beta3 subunit differentially modulates G-protein sensitivity of alpha1A and alpha1B Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  10. cAMP-dependent enhancement of dihydropyridine-sensitive calcium channel availability in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    Article
  11. Article
  12. Multiple components of Ca2+ channel facilitation in cerebellar granule cells: expression of facilitation during development in culture.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996
    Article
  13. Determinants of the G protein-dependent opioid modulation of neuronal calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Article
  14. ATP and G proteins affect the runup of the Ca2+ current in bovine chromaffin cells.Pflugers Archiv : European journal of physiology · 1995
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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

1 author at 1 institution in 1 country.

H KasaiAbteilung Membranbiophysik, Max-Planck-Institut für Biophysikalische Chemie, Göttingen, Federal Republic of Germany.
Max Planck Institute for Biophysical Chemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significant fraction of differentiated NG108-15 neuroblastoma/glioma cells have Ca2+ channel current different from that of undifferentiated cells. In the former cells, the Ca2+ channel sensitive to omega-conotoxin GVIA had slowed activation kinetics and was facilitated by depolarizing prepulses. These kinetic features are identical to those produced by inhibition of the channel by G proteins. Prolonged treatment with prostaglandin E1 and theophylline, agents that cause cellular differentiation, promoted incidence and extent of the tonic inhibition. Intracellular guanosine 5'-[beta-thio]diphosphate removed the tonic inhibition, suggesting sustained activation of a G protein, but pertussis toxin did not block it. A sulfhydryl alkylating agent, N-ethylmaleimide (0.1 mM), rapidly eliminated agonist-induced inhibition, whereas N-ethylmaleimide spared the tonic inhibition and the one induced by intracellular guanosine 5'-[gamma-thio]triphosphate. An agonist could further inhibit the Ca2+ channel that was already tonically inhibited. After washout of an inhibitory agonist, the tonic inhibition was temporarily removed. This "rebound facilitation" gradually faded within a few minutes. Pertussis toxin or N-ethylmaleimide prevented the rebound facilitation, whereas phorbol ester, forskolin, or arachidonic acid induced neither the rebound facilitation nor the tonic inhibition. Whatever its mechanism, the tonic inhibition of Ca2+ channels may serve as the basis for long-term and bidirectional regulation of activity of neuronal Ca2+ channels.

Indexed as

AnimalsCalcium ChannelsEnkephalin, D-Penicillamine (2,5)-EnkephalinsEthylmaleimideGTP-Binding ProteinsIn Vitro TechniquesMembrane PotentialsMollusk VenomsNeuroblastomaNeuronsPeptides, CyclicPertussis ToxinRatsTumor Cells, CulturedVirulence Factors, BordetellaCalcium ChannelsEnkephalin, D-Penicillamine (2,5)-EnkephalinsEthylmaleimideGTP-Binding ProteinsMollusk VenomsPeptides, CyclicPertussis ToxinVirulence Factors, Bordetella

Identifiers

PMID1656456
PMCPMC52609
OpenAlexW2040009964

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.