Evidence map›Paper›PMID 14507965›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Postsynaptic protein kinase A reduces neuronal excitability in response to increased synaptic excitation in the Drosophila CNS.

Richard A Baines

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Vesicular neurotransmitter transporters in Drosophila melanogaster.Biochimica et biophysica acta. Biomembranes · 2020
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Pumilio-2 regulates translation of Nav1.6 to mediate homeostasis of membrane excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  14. Activity-dependent alternative splicing increases persistent sodium current and promotes seizure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  15. Article
  16. Opportunities for text mining in the FlyBase genetic literature curation workflow.Database : the journal of biological databases and curation · 2012
    Article
  17. Endogenous patterns of activity are required for the maturation of a motor network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

1 author at 1 institution in 1 country.

Richard A BainesNeuroscience Group, Department of Biological Sciences, University of Warwick, Coventry, CV4 7AL, United Kingdom. RBaines@bio.warwick.ac.uk
University of Warwick · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Previous work has identified a role for synaptic activity in the development of excitable properties of motoneurons in the Drosophila embryo. In this study the underlying mechanism that enables two such neurons, termed aCC and RP2, to respond to increased exposure to synaptic excitation is characterized. Synaptic excitation is increased in genetic backgrounds that lack either a cAMP-specific phosphodiesterase (EC:3.1.4, dunce) or acetylcholinesterase (EC:3.1.1.7, ace), the enzyme that terminates the endogenous cholinergic excitation of these motoneurons. Analysis of membrane excitability in aCC/RP2, in either background, shows that these neurons have a significantly reduced capability to fire action potentials (APs) in response to injection of depolarizing current. Analysis of underlying voltage-gated currents show that this effect is associated with a marked reduction in magnitude of the voltage-dependent inward Na+ current (INa). Partially blocking INa in these motoneurons, using low concentrations of TTX, demonstrates that a reduction of INa is, by itself, sufficient to reduce membrane excitability. An analysis of firing implicates an increased AP threshold to underlie the reduction in membrane excitability observed because of heightened exposure to synaptic excitation. Genetic or pharmacological manipulations that either elevate cAMP or increase protein kinase A (PKA) activity in wild-type aCC/RP2 mimic both the reductions in membrane excitability and INa. In comparison, increasing cAMP catabolism or inhibition of PKA activity is sufficient to block the induction of these activity-dependent changes. The induced changes in excitability can be rapid, occurring within 5 min of exposure to a membrane-permeable cAMP analog, indicative that threshold can be regulated in these neurons by a post-translational mechanism that is dependent on phosphorylation.

Indexed as

3',5'-Cyclic-AMP PhosphodiesterasesAcetylcholinesteraseAction PotentialsAnimalsCell MembraneCentral Nervous SystemCyclic AMP-Dependent Protein KinasesDrosophilaDrosophila ProteinsElectric StimulationEmbryo, NonmammalianEnzyme InhibitorsGene Transfer TechniquesMotor NeuronsPatch-Clamp TechniquesSodium3',5'-Cyclic-AMP PhosphodiesterasesAcetylcholinesteraseCyclic AMP-Dependent Protein KinasesDrosophila ProteinsEnzyme InhibitorsSodium

Identifiers

PMID14507965
PMCPMC6740429
OpenAlexW2151968883

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.