Evidence map›Paper›PMID 33593855›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021

BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.

Zachary Niday, Bruce P Bean

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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  10. CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  20. Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024
    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.

Zachary NidayDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115.
Bruce P BeanDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115 bruce_bean@hms.harvard.edu.
Harvard University · US

Funding

VOLTAGE DEPENDENT ION CHANNELS IN PURKINJE NEURONSR01NS036855 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BEAN, BRUCE P · 1997 to 2022
$7.7M
Voltage-dependent ion channels in Purkinje neuronsR37NS036855 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BEAN, BRUCE P · 2002 to 2008
$2.8M
State-dependent interaction of antiepileptic drugs with voltage-dependent sodium channels and differential regulation of excitatory and inhibitory central neuronsR01NS110860 · NINDS · HARVARD MEDICAL SCHOOL · PI BEAN, BRUCE P · 2019 to 2022
$1.9M
NINDS NIH HHS R01 NS036855NINDS NIH HHS R01 NS110860NINDS NIH HHS R37 NS036855
6 · The paper itself

Abstract

BK calcium-activated potassium channels have complex kinetics because they are activated by both voltage and cytoplasmic calcium. The timing of BK activation and deactivation during action potentials determines their functional role in regulating firing patterns but is difficult to predict a priori. We used action potential clamp to characterize the kinetics of voltage-dependent calcium current and BK current during action potentials in Purkinje neurons from mice of both sexes, using acutely dissociated neurons that enabled rapid voltage clamp at 37°C. With both depolarizing voltage steps and action potential waveforms, BK current was entirely dependent on calcium entry through voltage-dependent calcium channels. With voltage steps, BK current greatly outweighed the triggering calcium current, with only a brief, small net inward calcium current before Ca-activated BK current dominated the total Ca-dependent current. During action potential waveforms, although BK current activated with only a short (∼100 μs) delay after calcium current, the two currents were largely separated, with calcium current flowing during the falling phase of the action potential and most BK current flowing over several milliseconds after repolarization. Step depolarizations activated both an iberiotoxin-sensitive BK component with rapid activation and deactivation kinetics and a slower-gating iberiotoxin-resistant component. During action potential firing, however, almost all BK current came from the faster-gating iberiotoxin-sensitive channels, even during bursts of action potentials. Inhibiting BK current had little effect on action potential width or a fast afterhyperpolarization but converted a medium afterhyperpolarization to an afterdepolarization and could convert tonic firing of single action potentials to burst firing.

Indexed as

Action PotentialsAnimalsCalciumCells, CulturedCerebellumFemaleLarge-Conductance Calcium-Activated Potassium ChannelsMaleMicePurkinje CellsSodium Channel BlockersCalciumLarge-Conductance Calcium-Activated Potassium ChannelsSodium Channel Blockersaction potential clampcalcium channelcerebellumiberiotoxinKCa1.1paxilline

Identifiers

PMID33593855
PMCPMC8018884
OpenAlexW3132507685

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.