Evidence map›Paper›PMID 10377341›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Voltage-dependent neuromodulation of Na+ channels by D1-like dopamine receptors in rat hippocampal neurons.

A R Cantrell, T Scheuer, W A Catterall

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Regulation of α-cell glucagon secretion: The role of second messengers.Chronic diseases and translational medicine · 2022
    Review
  5. Article
  6. Article
  7. Altered gating of KeLife · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Regulation of sodium channel activity by phosphorylation.Seminars in cell & developmental biology · 2011
    Review
  15. Review
  16. Review
  17. Short trains of theta frequency stimulation enhance CA1 pyramidal neuron excitability in the absence of synaptic potentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  18. Article
  19. Article
  20. State-dependent modulation of amygdala inputs by dopamine-induced enhancement of sodium currents in layer V entorhinal cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    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.

A R CantrellDepartment of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA.
T Scheuer
W A Catterall
University of Washington · US

Funding

VOLTAGE-SENSITIVE SODIUM CHANNELS IN BRAINR01NS015751 · NINDS · UNIVERSITY OF WASHINGTON · PI CATTERALL, WILLIAM A · 1985 to 2018
$6.0M
NINDS NIH HHS NS10147NINDS NIH HHS NS15751
6 · The paper itself

Abstract

Activation of D1-like dopamine (DA) receptors reduces peak Na+ current in acutely isolated hippocampal neurons through phosphorylation of the alpha subunit of the Na+ channel by cAMP-dependent protein kinase (PKA). Here we report that neuromodulation of Na+ currents by DA receptors via PKA is voltage-dependent in the range of -110 to -70 mV and is also sensitive to concurrent activation of protein kinase C (PKC). Depolarization enhanced the ability of D1-like DA receptors to reduce peak Na+ currents via the PKA pathway. Similar voltage-dependent modulation was observed when PKA was activated directly with the membrane-permeant PKA activator DCl-cBIMPS (cBIMPS; 20 microM), indicating that the membrane potential dependence occurs downstream of PKA. PKA activation caused only a small (-2.9 mV) shift in the voltage dependence of steady-state inactivation and had no effect on slow inactivation or on the rates of entry into the fast or slow inactivated states, suggesting that another mechanism is responsible for coupling of membrane potential changes to PKA modulation. Activation of PKC with a low concentration of the membrane-permeant diacylglycerol analog oleylacetyl glycerol also potentiated modulation by SKF 81297 or cBIMPS, and these effects were most striking at hyperpolarized membrane potentials where PKA modulation was not stimulated by membrane depolarization. Thus, activation of D1-like DA receptors causes a strong reduction in Na+ current via the PKA pathway, but it is effective primarily when it is combined with depolarization or activation of PKC. The convergence of these three distinct signaling modalities on the Na+ channel provides an intriguing mechanism for integration of information from multiple signaling pathways in the hippocampus and CNS.

Indexed as

Ion Channel GatingAnimalsBenzazepinesCalciumCell LineCells, CulturedCyclic AMP-Dependent Protein KinasesDiphosphonatesDopamine AgonistsEnzyme ActivationHumansIn Vitro TechniquesMaleMembrane PotentialsPhosphorylationProtein Kinase CBenzazepinesbis(isopropyl methyl)phosphonateCalciumCyclic AMP-Dependent Protein KinasesDiphosphonatesDopamine AgonistsProtein Kinase CReceptors, Dopamine D1SK&F 81297SodiumSodium Channels

Identifiers

PMID10377341
PMCPMC6782346
OpenAlexW1591245254

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.