Evidence map›Paper›PMID 9801357›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Heterologous expression of the Kv3.1 potassium channel eliminates spike broadening and the induction of a depolarizing afterpotential in the peptidergic bag cell neurons.

M D Whim, L K Kaczmarek

Open access · bronzeAbstract read
PubMed Full text at PMC
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 27 citations in OpenAlex.

  1. Protein Kinase C Enhances Electrical Synaptic Transmission by Acting on Junctional and Postsynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  2. Article
  3. Separate Ca2+ sources are buffered by distinct Ca2+ handling systems in aplysia neuroendocrine cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  4. Fragile X mental retardation protein is required for rapid experience-dependent regulation of the potassium channel Kv3.1b.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  5. Article
  6. Prolonged activation of Ca2+-activated K+ current contributes to the long-lasting refractory period of Aplysia bag cell neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  7. Article
  8. Article
  9. Coregulation of voltage-dependent kinetics of Na(+) and K(+) currents in electric organ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    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

2 authors at 1 institution in 1 country.

M D WhimDepartment of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520-8066, USA.
L K Kaczmarek
Yale University · US

Funding

Biochemical Control of Excitibility in NeuronsR01NS018492 · NINDS · YALE UNIVERSITY · PI KACZMAREK, LEONARD K · 1985 to 2010
$3.6M
NINDS NIH HHS NS-18492NINDS NIH HHS R01 NS018492
6 · The paper itself

Abstract

The bag cell neurons of Aplysia are a cluster of cells that control egg laying behavior. After brief synaptic stimulation, they depolarize and fire spontaneously for up to 30 min. During the first few seconds of this afterdischarge, the action potentials of the bag cell neurons undergo pronounced broadening. Single bag cell neurons in culture also show spike broadening in response to repeated depolarizations. This broadening is frequency-dependent and associated with the induction of a depolarizing afterpotential lasting minutes. In some neurons the depolarizing afterpotential is sufficient to trigger spontaneous firing. To test the possibility that spike broadening during stimulation is required to trigger the depolarizing afterpotential, we eliminated frequency-dependent broadening by heterologous expression of the Kv3.1 potassium channel. This channel has rapid activation and deactivation kinetics and no use-dependent inactivation. Expression of Kv3.1 prevented spike broadening and also eliminated the depolarizing afterpotential. Measurements of the integral of calcium current during voltage commands, which simulated the action potentials of the control neurons and those expressing Kv3.1, indicate that spike broadening produces up to a fivefold increase in calcium entry. Manipulations that limit calcium entry during action potentials or chelation of intracellular calcium using BAPTA AM prevented the induction of the depolarizing afterpotential. We conclude that spike broadening is essential for the induction of the depolarizing afterpotential probably by regulating calcium influx and suggest that one of the physiological roles of spike broadening may be to regulate long-term changes in neuronal excitability.

Indexed as

Potassium Channels, Voltage-GatedAction PotentialsAnimalsAplysiaCalciumChelating AgentsEgtazic AcidGene ExpressionMagnesiumNeuronsNeuropeptidesPatch-Clamp TechniquesPlasmidsPotassium ChannelsRefractory Period, ElectrophysiologicalShaw Potassium Channels1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl esterCalciumChelating AgentsEgtazic AcidMagnesiumNeuropeptidesPotassium ChannelsPotassium Channels, Voltage-GatedShaw Potassium ChannelsTetraethylammonium

Identifiers

PMID9801357
PMCPMC6792887
OpenAlexW2146344006

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.