Evidence map›Paper›PMID 15034127›Full record

ArticleThe Journal of physiology2004

BK potassium channels control transmitter release at CA3-CA3 synapses in the rat hippocampus.

Giacomo Raffaelli, Chiara Saviane, Majid H Mohajerani, Paola Pedarzani, Enrico Cherubini

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

117 citing papers in PubMed, 194 citations in OpenAlex.

  1. Article
  2. Article
  3. 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
  4. Article
  5. Article
  6. Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024
    Review
  7. Review
  8. CaInternational journal of molecular sciences · 2023
    Review
  9. Regulation of Neurotransmitter Release by KAdvances in neurobiology · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Mitochondrial BKFrontiers in physiology · 2021
    Article
  19. Review
  20. Article

57 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

5 authors at 2 institutions in 2 countries.

Giacomo RaffaelliNeuroscience Program, International School for Advanced Studies (SISSA), Via Beirut 2-4, 34014 Trieste, Italy.
Chiara Saviane
Majid H Mohajerani
Paola Pedarzani
Enrico Cherubini
Scuola Internazionale Superiore di Studi Avanzati · ITUniversity College London · GB

Funding

Medical Research Council G0100066
6 · The paper itself

Abstract

Large conductance calcium- and voltage-activated potassium channels (BK channels) activate in response to calcium influx during action potentials and contribute to the spike repolarization and fast afterhyperpolarization. BK channels targeted to active zones in presynaptic nerve terminals have been shown to limit calcium entry and transmitter release by reducing the duration of the presynaptic spike at neurosecretory nerve terminals and at the frog neuromuscular junction. However, their functional role in central synapses is still uncertain. In the hippocampus, BK channels have been proposed to act as an 'emergency brake' that would control transmitter release only under conditions of excessive depolarization and accumulation of intracellular calcium. Here we demonstrate that in the CA3 region of hippocampal slice cultures, under basal experimental conditions, the selective BK channel blockers paxilline (10 microM) and iberiotoxin (100 nM) increase the frequency, but not the amplitude, of spontaneously occurring action potential-dependent EPSCs. These drugs did not affect miniature currents recorded in the presence of tetrodotoxin, suggesting that their action was dependent on action potential firing. Moreover, in double patch-clamp recordings from monosynaptically interconnected CA3 pyramidal neurones, blockade of BK channels enhanced the probability of transmitter release, as revealed by the increase in success rate, EPSC amplitude and the concomitant decrease in paired-pulse ratio in response to pairs of presynaptic action potentials delivered at a frequency of 0.05 Hz. BK channel blockers also enhanced the appearance of delayed responses, particularly following the second action potential in the paired-pulse protocol. These results are consistent with the hypothesis that BK channels are powerful modulators of transmitter release and synaptic efficacy in central neurones.

Indexed as

Action PotentialsAnimalsElectrophysiologyExcitatory Postsynaptic PotentialsGlutamic AcidHippocampusIndolesKv1.1 Potassium ChannelMembrane PotentialsNeuronsNeurotransmitter AgentsOrgan Culture TechniquesPatch-Clamp TechniquesPeptidesPotassium Channel BlockersPotassium Channels, Voltage-GatedGlutamic AcidiberiotoxinIndolesKcna1 protein, ratKv1.1 Potassium ChannelNeurotransmitter AgentspaxillinePeptidesPotassium Channel BlockersPotassium Channels, Voltage-Gated

Identifiers

PMID15034127
PMCPMC1665041
OpenAlexW1604744466

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.