Evidence map›Paper›PMID 15201332›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Paradoxical potentiation of neuronal T-type Ca2+ current by ATP at resting membrane potential.

Nathalie Leresche, Julien Hering, Régis C Lambert

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. The Augmentation of Retinogeniculate Communication during Thalamic Burst Mode.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  4. Sub-synaptic localization of CaBrain structure & function · 2017
    Article
  5. Article
  6. Article
  7. Article
  8. T-type Ca2+ channels in absence epilepsy.Pflugers Archiv : European journal of physiology · 2014
    Review
  9. The many faces of T-type calcium channels.Pflugers Archiv : European journal of physiology · 2014
    Review
  10. Article
  11. T-type calcium channels consolidate tonic action potential output of thalamic neurons to neocortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  12. Article
  13. Bidirectional plasticity in the primate inferior olive induced by chronic ethanol intoxication and sustained abstinence.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  14. Article
  15. Manipulation of adenosine kinase affects sleep regulation in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

3 authors.

Nathalie LerescheNeurobiologie des Processus Adaptatifs, Unité Mixte de Recherche (UMR) 7102 Centre National de la Recherche Scientifique, Université Paris 6, 75252 Paris Cedex 05, France.
Julien Hering
Régis C Lambert

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the marked influence on neuronal physiology of the low-voltage activated T-type Ca(2+) currents, little is known about the intracellular pathways and neurotransmitters involved in their regulations. Here, we report that in thalamocortical neurons a phosphorylation mechanism induces an increase both in the current amplitude (1.5 +/- 0.27-fold in the ventrobasal nucleus) and its inactivation kinetics. Dialysis of the neuron with an ATP-free solution suppresses the T-current potentiation, whereas it becomes irreversible in the presence of ATPgammaS. Phosphorylation occurs when the channels are inactivated and is slowly removed when they recover from inactivation and remain in closed states (time constants of the induction and removal of the potentiation: 579 +/- 143 msec and 4.9 +/- 1.1 sec, respectively, at 25 degrees C). The resulting apparent voltage sensitivity of this regulation follows the voltage dependence of the current steady-state inactivation. Thus, the current is paradoxically inhibited when the preceding hyperpolarization is lengthened, and maximal currents are generated after transient hyperpolarizations with a duration (0.7-1.5 sec) that is defined by the balance between the kinetics of the dephosphorylation and deinactivation. In addition, the phosphorylation will facilitate the generation of T current at resting membrane potential. This potentiation, which is specific to sensory thalamocortical neurons, would markedly influence the electroresponsiveness of these neurons and represent the first evidence of a regulation of native Cav3.1 channels.

Indexed as

Adenosine TriphosphateAnimalsCalcium Channels, T-TypeImmunohistochemistryIn Vitro TechniquesIon Channel GatingKineticsMembrane PotentialsNeuronsPatch-Clamp TechniquesPhosphorylationRatsRats, WistarThalamusAdenosine TriphosphateCalcium Channels, T-Type

Identifiers

PMID15201332
PMCPMC6729316

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.