Evidence map›Paper›PMID 11739569›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Presynaptic Ca2+-activated K+ channels in glutamatergic hippocampal terminals and their role in spike repolarization and regulation of transmitter release.

H Hu, L R Shao, S Chavoshy, N Gu, M Trieb, R Behrens, P Laake, O Pongs, H G Knaus, O P Ottersen and 1 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

181 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. The role of Botulinum Toxin for the Management of post Parotidectomy Sialocele: A Randomized Controlled Trial.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025
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  12. BK channels mediate a presynaptic form of mGluR-LTD in the neonatal hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. BK Channelopathies andAnnual review of physiology · 2024
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  14. Article
  15. Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024
    Review
  16. BK channels sustain neuronal CaCellular and molecular life sciences : CMLS · 2023
    Article
  17. CaInternational journal of molecular sciences · 2023
    Review
  18. KCurrent neuropharmacology · 2023
    Review
  19. Regulation of Neurotransmitter Release by KAdvances in neurobiology · 2023
    Article
  20. Article

121 more citing papers are in PubMed but not listed here.

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

11 authors.

H HuInstitute of Physiology, University of Oslo, Blindern, N-0317 Oslo, Norway.
L R Shao
S Chavoshy
N Gu
M Trieb
R Behrens
P Laake
O Pongs
H G Knaus
O P Ottersen
J F Storm

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Large-conductance Ca(2+)-activated K(+) channels (BK, also called Maxi-K or Slo channels) are widespread in the vertebrate nervous system, but their functional roles in synaptic transmission in the mammalian brain are largely unknown. By combining electrophysiology and immunogold cytochemistry, we demonstrate the existence of functional BK channels in presynaptic terminals in the hippocampus and compare their functional roles in somata and terminals of CA3 pyramidal cells. Double-labeling immunogold analysis with BK channel and glutamate receptor antibodies indicated that BK channels are targeted to the presynaptic membrane facing the synaptic cleft in terminals of Schaffer collaterals in stratum radiatum. Whole-cell, intracellular, and field-potential recordings from CA1 pyramidal cells showed that the presynaptic BK channels are activated by calcium influx and can contribute to repolarization of the presynaptic action potential (AP) and negative feedback control of Ca(2+) influx and transmitter release. This was observed in the presence of 4-aminopyridine (4-AP, 40-100 microm), which broadened the presynaptic compound action potential. In contrast, the presynaptic BK channels did not contribute significantly to regulation of action potentials or transmitter release under basal experimental conditions, i.e., without 4-AP, even at high stimulation frequencies. This is unlike the situation in the parent cell bodies (CA3 pyramidal cells), where BK channels contribute strongly to action potential repolarization. These results indicate that the functional role of BK channels depends on their subcellular localization.

Indexed as

4-AminopyridineAction PotentialsAnimalsElectric StimulationExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGlutamic AcidHippocampusImmunohistochemistryIn Vitro TechniquesLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsLarge-Conductance Calcium-Activated Potassium ChannelsMaleNeurotransmitter AgentsPatch-Clamp TechniquesPotassium Channel Blockers4-AminopyridineExcitatory Amino Acid AntagonistsGlutamic AcidKcnma1 protein, ratLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsLarge-Conductance Calcium-Activated Potassium ChannelsNeurotransmitter AgentsPotassium Channel BlockersPotassium ChannelsPotassium Channels, Calcium-ActivatedReceptors, N-Methyl-D-Aspartate

Identifiers

PMID11739569
PMCPMC6763057

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.