Evidence map›Paper›PMID 12882229›Full record

ReviewCerebellum (London, England)2003

Expression and distribution of voltage-gated sodium channels in the cerebellum.

Kristin L Schaller, John H Caldwell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cerebellum (London, England), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

65 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. NaThe Journal of comparative neurology · 2026
    Article
  3. Article
  4. Channels (Austin, Tex.) · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. [Expression changes of NaNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  9. Article
  10. Review
  11. Social Deficits and Cerebellar Degeneration in Purkinje CellFrontiers in molecular neuroscience · 2022
    Article
  12. Article
  13. Article
  14. Properties of Calmodulin Binding to NaNeurochemical research · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

5 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

2 authors at 1 institution in 1 country.

Kristin L SchallerDepartment of Cellular and Structural Biology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
John H Caldwell
University of Colorado Health · US

Funding

ION CHANNELS IN THE NERVOUS SYSTEMR01NS026505 · NINDS · UNIVERSITY OF COLORADO DENVER · PI CALDWELL, JOHN H · 1989 to 2003
$1.2M
NINDS NIH HHS NS R01 26505
6 · The paper itself

Abstract

In order to understand the effects of sodium channels on synaptic signaling and response in the cerebellum, it is essential to know for each class of neuron what sodium channel isoforms are present, and the properties and distribution of each. Sodium channels are heteromultimeric membrane proteins, consisting of a large alpha subunit that forms the pore, and one or more beta subunits. Ten genes encode an alpha subunit in mammals, and of these, four are expressed in the cerebellum: Nav1.1, Nav1.2, Nav1.3 and Nav1.6. Three genes encode beta subunits (Nabeta1-3), and all three are expressed in the cerebellum. However, Nav1.3 and Nabeta3 have been found only in the developing cerebellum. All sodium channels recorded in the cerebellum are TTX-sensitive with similar kinetics, making it difficult to identify the isoforms electrically. Thus, most of the expression studies have relied on techniques that allow visualization of sodium channel subtypes at the level of mRNA and protein. In situ hybridization and immunolocalization studies demonstrated that granule cells predominantly express Nav1.2, Nav1.6, Nabeta1, and Nabeta2. Protein for Nav1.2 and Nav1.6 is localized primarily in granule cell parallel fibers. Purkinje cells express Nav1.1, Nav1.6, Nabeta1 and Nabeta2. The somato-dendritic localization of Nav1.1 and Nav1.6 in Purkinje cells suggests that these isoforms are involved in the integration of synaptic input. Deep cerebellar nuclei neurons expressed Nav1.1 and Nav1.6 as well as Nabeta1. Bergmann glia expressed Nav1.6, but not granule cell layer astrocytes. Some sodium channel isoforms that are not expressed normally in the adult cerebellum are expressed in animals with mutations or disease. Electrophysiological studies suggest that Nav1.6 is responsible for spontaneous firing and bursting features in Purkinje cells, but the specialized functions of the other subunits in the cerebellum remain unknown.

Indexed as

AnimalsCerebellumHumansNeuronsPotassium Channels, Voltage-GatedPurkinje CellsPotassium Channels, Voltage-Gated

Identifiers

PMID12882229
OpenAlexW2039398588

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.