Evidence map›Paper›PMID 16901946›Full record

ArticleThe Journal of physiology2006

Kinetics of ion channel modulation by cAMP in rat hippocampal neurones.

Barrie Lancaster, Hua Hu, Barry Gibb, Johan F Storm

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.4field-weighted citation impact, top 51% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Cellular mechanisms underlying spatiotemporal features of cholinergic retinal waves.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  11. Article
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  13. Article
  14. Type 4 phosphodiesterase plays different integrating roles in different cellular domains in pyramidal cortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  15. Learning-related postburst afterhyperpolarization reduction in CA1 pyramidal neurons is mediated by protein kinase A.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  16. Dynamics of protein kinase A signaling at the membrane, in the cytosol, and in the nucleus of neurons in mouse brain slices.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

4 authors at 2 institutions in 2 countries.

Barrie LancasterWolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. b.lancaster@ucl.ac.uk
Hua Hu
Barry Gibb
Johan F Storm
University College London · GBUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ion channel regulation by cyclic AMP and protein kinase A is a major effector mechanism for monoamine transmitters and neuromodulators in the CNS. Surprisingly, there is little information about the speed and kinetic limits of cAMP-PKA-dependent excitability changes in the brain. To explore these questions, we used flash photolysis of caged-cAMP (DMNB-cAMP) to provide high temporal resolution. The resultant free cAMP concentration was calculated from separate experiments in which this technique was used, in excised patches, to activate cAMP-sensitive cyclic nucleotide-gated (CNG) channels expressed in Xenopus oocytes. In hippocampal pyramidal neurones we studied the modulation of a potassium current (slow AHP current, I(sAHP)) known to be targeted by multiple transmitter systems that use cAMP-PKA. Rapid cAMP elevation by flash photolyis of 200 microm DMNB-cAMP completely inhibited the K(+) current. The estimated yield (1.3-3%) suggests that photolysis of 200 microm caged precursor is sufficient for full PKA activation. By contrast, extended gradual photolysis of 200 microm DMNB-cAMP caused stable but only partial inhibition. The kinetics of rapid cAMP inhibition of the K(+) conductance (time constant 1.5-2 s) were mirrored by changes in firing patterns commencing within 500 ms of rapid cAMP elevation. Maximal increases in firing were short-lasting (< 60 s) and gave way to moderately enhanced levels of spiking. The results demonstrate how the fidelity of phasic monoamine signalling can be preserved by the cAMP-PKA pathway.

Indexed as

Action PotentialsAnimalsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsFemaleGene Expression RegulationHippocampusIon Channel GatingIon ChannelsKineticsNeuronsPatch-Clamp TechniquesPhotolysisPotassium Channels, Calcium-ActivatedPyramidal CellsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsIon ChannelsPotassium Channels, Calcium-Activated

Identifiers

PMID16901946
PMCPMC1890347
OpenAlexW1576979528

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.