Evidence map›Paper›PMID 18983899›Full record

ArticleNeuroscience2009

T-type calcium channels mediate rebound firing in intact deep cerebellar neurons.

K Alviña, G Ellis-Davies, K Khodakhah

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2009. 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
2.6field-weighted citation impact, top 10% 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, 58 citations in OpenAlex.

  1. Review
  2. Cerebellar Functions Beyond Movement and Learning.Annual review of neuroscience · 2024
    Review
  3. Review
  4. Article
  5. Differential Coding Strategies in Glutamatergic and GABAergic Neurons in the Medial Cerebellar Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. The cerebellar nuclei take center stage.Cerebellum (London, England) · 2011
    Article
  19. Review
  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 at 2 institutions in 2 countries.

K AlviñaDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, 1410 Pelham Parkway South, Kennedy Center Room 506, Bronx, NY 10461, USA.
G Ellis-Davies
K Khodakhah
John F. Kennedy Center for the Performing Arts · USDrexel University · US

Funding

PHOTOCHEMICAL REGULATION OF CALCIUM IN CELL PHYSIOLOGYR01GM053395 · NIGMS · OREGON HEALTH AND SCIENCE UNIVERSITY · PI ELLIS-DAVIES, GRAHAM · 1995 to 2020
$6.1M
Cerebellar Function in Health and DiseaseR01NS050808 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI KHODAKHAH, KAMRAN · 2006 to 2016
$3.9M
NIGMS NIH HHS R01 GM053395NINDS NIH HHS R01 NS050808
6 · The paper itself

Abstract

Neurons of the deep cerebellar nuclei (DCN) form the main output of the cerebellar circuitry and thus play an important role in cerebellar motor coordination. A prominent biophysical property observed in rat DCN neurons is rebound firing; a brief but strong hyperpolarizing input transiently increases their firing rate to much higher levels compared with that prior to the inhibitory input. Low-threshold T-type voltage-gated calcium channels have been suspected for a long time to be responsible for this phenomenon, but direct pharmacological evidence in support of this proposition is lacking. Even though a multitude of functional roles has been assigned to rebound firing in DCN neurons, their prevalence under physiological conditions is in question. Studies aimed at delineating the physiological role of rebound firing are hampered by the lack of a good pharmacological blocker. Here we show that mibefradil, a compound that blocks T-type calcium channels, potently blocks rebound firing in DCN neurons. In whole-cell experiments both mibefradil and NNC 55-0396 [(1S,2S)-2-(2-(N-[(3-benzimidazol-2-yl)propyl]-N-methylamino)ethyl)-6-fluoro-1,2,3,4-tetrahydro-1-isopropyl-2-naphtyl cyclopropanecarboxylate dihydrochloride]. a more selective T-type calcium channel blocker, effectively blocked rebound firing produced by direct current injection. Thus, mibefradil and other T-type channel modulators may prove to be invaluable tools for elucidating the functional importance of DCN rebound firing in cerebellar computation.

Indexed as

Action PotentialsAnimalsAnimals, NewbornCalcium Channel BlockersCalcium Channels, T-TypeCerebellumDrug InteractionsElectric Stimulationgamma-Aminobutyric AcidIn Vitro TechniquesMibefradilNeural InhibitionNeuronsPatch-Clamp TechniquesRatsRats, WistarCalcium Channel BlockersCalcium Channels, T-Typegamma-Aminobutyric AcidMibefradil

Identifiers

PMID18983899
PMCPMC2649676
OpenAlexW2024239821

What OpenQuestion holds

Textmetadata
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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.