Evidence map›Paper›PMID 11850502›Full record

ArticleThe Journal of physiology2002

Phasic and tonic attenuation of EPSPs by inward rectifier K+ channels in rat hippocampal pyramidal cells.

Tomoko Takigawa, Christian Alzheimer

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

39 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  6. Neuronal Chloride Regulation via KCC2 Is Modulated through a GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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  13. Inward-rectifying potassium (Kir) channels regulate pacemaker activity in spinal nociceptive circuits during early life.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  14. Article
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  16. IRK-1 potassium channels mediate peptidergic inhibition of Caenorhabditis elegans serotonin neurons via a G(o) signaling pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. Article
  18. Adenosine release during seizures attenuates GABAA receptor-mediated depolarization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
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  20. Review
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.

Tomoko TakigawaDepartment of Physiology, University of Munich, Pettenkoferstr. 12, 80336 Munich, Germany.
Christian Alzheimer
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We made whole-cell recordings from CA1 pyramidal cells of hippocampal slices in combination with brief dendritic glutamate pulses to study the role of constitutive inwardly rectifying K+ channels (IRK, Kir2.0) and G-protein-activated inwardly rectifying K+ channels (GIRK, Kir3.0) in the processing of excitatory inputs. Phasic activation of GIRK channels by baclofen (20 microM) produced a reversible reduction of glutamate-evoked postsynaptic potentials (GPSPs), our equivalent of EPSPs, by about one-third. Conversely, tertiapin (30 nM), a selective inhibitor of GIRK channels, and Ba2+ (200 microM), a non-selective blocker of inwardly rectifying K+ channels, enhanced GPSPs and, in voltage-clamp experiments, reduced the underlying K+ conductances, indicating a functionally significant background GIRK conductance, in addition to constitutive IRK channel activity. When examined after suppression of endogenous adenosinergic inhibition, using either adenosine deaminase or the selective A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine, tertiapin failed to influence either the GPSPs or the inwardly rectifying K+ conductance. Voltage-clamp recordings from acutely isolated CA1 pyramidal cells not exposed to ambient adenosine exhibited no response to tertiapin, whereas Ba2+ was still capable of reducing hyperpolarizing inward rectification. Our data indicate that in hippocampal pyramidal cells, two components of the inwardly rectifying K+ conductance can be identified, which together exert a tonic modulation of excitatory synaptic input: one arises from constitutive putative IRK channels, the other is mediated by the background activity of GIRK channels that results from the tonic activation of A1 receptors by ambient adenosine.

Indexed as

AnimalsElectrophysiologyExcitatory Postsynaptic PotentialsG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHippocampusIn Vitro TechniquesPotassium ChannelsPotassium Channels, Inwardly RectifyingPyramidal CellsRatsRats, WistarG Protein-Coupled Inwardly-Rectifying Potassium ChannelsPotassium ChannelsPotassium Channels, Inwardly Rectifying

Identifiers

PMID11850502
PMCPMC2290130
OpenAlexW2002965269

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.