Evidence map›Paper›PMID 26969302›Full record

ReviewThe Journal of physiology2016

Presynaptic BK channels control transmitter release: physiological relevance and potential therapeutic implications.

Marilena Griguoli, Martina Sgritta, Enrico Cherubini

Abstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

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

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Therapeutic efficacy of the BKCa channel opener chlorzoxazone in a mouse model of Fragile X syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024
    Review
  14. Article
  15. Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024
    Article
  16. Review
  17. Review
  18. CaInternational journal of molecular sciences · 2023
    Review
  19. Rufinamide, a Triazole-Derived Antiepileptic Drug, Stimulates CaInternational journal of molecular sciences · 2022
    Article
  20. 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

3 authors.

Marilena GriguoliEuropean Brain Research Institute (EBRI) 'Fondazione Rita Levi-Montalcini', Via del Fosso di Fiorano 64, 00143, Rome, Italy.ORCID 0000-0003-4067-8927
Martina SgrittaEuropean Brain Research Institute (EBRI) 'Fondazione Rita Levi-Montalcini', Via del Fosso di Fiorano 64, 00143, Rome, Italy.
Enrico CherubiniEuropean Brain Research Institute (EBRI) 'Fondazione Rita Levi-Montalcini', Via del Fosso di Fiorano 64, 00143, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BK channels are large conductance potassium channels characterized by four pore-forming α subunits, often co-assembled with auxiliary β and γ subunits to regulate Ca(2+) sensitivity, voltage dependence and gating properties. Abundantly expressed in the CNS, they have the peculiar characteristic of being activated by both voltage and intracellular calcium rise. The increase in intracellular calcium via voltage-dependent calcium channels (Cav ) during spiking triggers conformational changes and BK channel opening. This narrows the action potential and induces a fast after-hyperpolarization that shuts calcium channels. The tight coupling between BK and Cav channels at presynaptic active zones makes them particularly suitable for regulating calcium entry and neurotransmitter release. While in most synapses, BK channels exert a negative control on transmitter release under basal conditions, in others they do so only under pathological conditions, serving as an emergency brake to protect against hyperactivity. In particular cases, by interacting with other channels (i.e. limiting the activation of the delayed rectifier and the inactivation of Na(+) channels), BK channels induce spike shortening, increase in firing rate and transmitter release. Changes in transmitter release following BK channel dysfunction have been implicated in several neurological disorders including epilepsy, schizophrenia, fragile X syndrome, mental retardation and autism. In particular, two mutations, one in the α and one in the β3 subunit, resulting in a gain of function have been associated with epilepsy. Hence, these discoveries have allowed identification of BK channels as new drug targets for therapeutic intervention.

Indexed as

AnimalsHumansLarge-Conductance Calcium-Activated Potassium ChannelsNeurotransmitter AgentsPresynaptic TerminalsSynaptic TransmissionLarge-Conductance Calcium-Activated Potassium ChannelsNeurotransmitter Agents

Identifiers

PMID26969302
PMCPMC4929328

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.