Evidence map›Paper›PMID 10436040›Full record

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

Modulation of a slowly inactivating potassium current, I(D), by metabotropic glutamate receptor activation in cultured hippocampal pyramidal neurons.

R L Wu, M E Barish

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Potassium currents during the action potential of hippocampal CA3 neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  13. Article
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  15. Modulation of excitability by alpha-dendrotoxin-sensitive potassium channels in neocortical pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  16. Group I metabotropic glutamate receptors elicit epileptiform discharges in the hippocampus through PLCbeta1 signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  17. 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 2 institutions in 1 country.

R L WuDivision of Neurosciences, Beckman Research Institute of the City of Hope, Duarte, California 91010, USA.
M E Barish
Beckman Research InstituteCity of Hope · US

Funding

DIFFERENTIATION OF NEURONAL SIGNALING MECHANISMSR01NS023857 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI BARISH, MICHAEL E · 1986 to 2000
$253k
NINDS NIH HHS R01 NS23857
6 · The paper itself

Abstract

I(D) is a slowly inactivating 4-aminopyridine (4-AP)-sensitive potassium current of hippocampal pyramidal neurons and other CNS neurons. Although I(D) exerts multifaceted influence on CNS excitability, whether I(D) is subject to modulation by neurotransmitters or neurohormones has not been clear. We report here that one prominent effect of metabotropic glutamate receptor (mGluR) activation by short (3 min) exposure to 1S, 3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (100 microM) is suppression of I(D) by acceleration of its inactivation. I(D) was identified as a target of mGluR-mediated modulation because inactivation of a component of outward current sensitive to 100-200 microM 4-AP was accelerated by 1S,3R-ACPD, and because 4-AP occluded any further actions of 1S,3R-ACPD. Enhancement of I(D) inactivation was induced by the group I-preferring agonist RS-3, 5-dihydroxyphenylglycine (3,5-DHPG) and the group II-preferring agonist 2S,2'R,3'R)-2-(2',3'dicarboxycyclopropyl)-glycine (DCG-IV), but not by the group III-preferring agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4); it was blocked by the broadly acting mGluR antagonist S-alpha-methyl-4-carboxyphenylglycine (S-MCPG). Furthermore, inactivation of I(D) was enhanced by inclusion of GTPgammaS in the internal solution and blocked by inclusion of GDPbetaS. Metabotropic GluR-induced suppression of I(D) was manifest in three aspects of excitability previously linked to I(D) by their sensitivity to 4-AP: reduction in input conductance and enhanced excitability at voltages just positive to the resting potential, reduced delay to action potential firing during depolarizing current injections, and delayed action potential repolarization. We suggest that mGluR-induced suppression of I(D) could contribute to enhancement of hippocampal neuron excitability and synaptic connections.

Indexed as

Action PotentialsAnimalsCells, CulturedCycloleucineElectric ConductivityGTP-Binding ProteinsMembrane PotentialsMicePatch-Clamp TechniquesPotassium ChannelsPyramidal CellsReceptors, Metabotropic GlutamateTime Factors1-amino-1,3-dicarboxycyclopentaneCycloleucineGTP-Binding ProteinsPotassium ChannelsReceptors, Metabotropic Glutamate

Identifiers

PMID10436040
PMCPMC6782886
OpenAlexW1922134188

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.