Evidence map›Paper›PMID 16690702›Full record

ArticleThe Journal of physiology2006

Ionic mechanisms of autorhythmic firing in rat cerebellar Golgi cells.

Lia Forti, Elisabetta Cesana, Jonathan Mapelli, Egidio D'Angelo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

89 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Effects of Short-Term Synaptic Plasticity in Feedforward Inhibitory Circuits on Cerebellar Responses to Repetitive Sensory Input.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  3. Tremor pathophysiology.Clinical parkinsonism & related disorders · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Calcium Channel-Dependent Induction of Long-Term Synaptic Plasticity at Excitatory Golgi Cell Synapses of Cerebellum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Acetylcholine Modulates Cerebellar Granule Cell Spiking by Regulating the Balance of Synaptic Excitation and Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  20. Article

29 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

4 authors at 3 institutions in 1 country.

Lia FortiDipartimento di Scienze Fisiologiche e Farmacologiche, Università di Pavia, Via Forlanini 6, 27100 Pavia, Italy. lforti@unipv.it
Elisabetta Cesana
Jonathan Mapelli
Egidio D'Angelo
Fondazione Istituto Neurologico Nazionale Casimiro Mondino · ITIstituto Nazionale per la Fisica della Materia · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Golgi cells (GoCs), the main type of inhibitory interneuron in the cerebellar granular layer (GL), are thought to play a central role in cerebellar network function, their excitable properties have remained unexplored. GoCs fire rhythmically in vivo and in slices, but it was unclear whether this activity originated from pacemaker ionic mechanisms. We explored this issue in acute cerebellar slices from 3-week-old rats by combining loose cell-attached (LCA) and whole-cell (WC) recordings. GoCs displayed spontaneous firing at 1-10 Hz (room temperature) and 2-20 Hz (35-37 degrees C), which persisted in the presence of blockers of fast synaptic receptors and mGluR and GABAB receptors, thus behaving, in our conditions, as pacemaker neurons. ZD 7288 (20 microM), a potent hyperpolarization-activated current (Ih) blocker, slowed down pacemaker frequency. The role of subthreshold Na+ currents (INa,sub) could not be tested directly, but we observed a robust TTX-sensitive, non-inactivating Na+ current in the subthreshold voltage range. When studying repolarizing currents, we found that retigabine (5 microM), an activator of KCNQ K+ channels generating neuronal M-type K+ (IM) currents, reduced GoC excitability in the threshold region. The KCNQ channel antagonist XE991 (5 microM) did not modify firing, suggesting that GoC IM has low XE991 sensitivity. Spike repolarization was followed by an after-hyperpolarization (AHP) supported by apamin-sensitive Ca2+-dependent K+ currents (I(apa)). Block of I(apa) decreased pacemaker precision without altering average frequency. We propose that feed-forward depolarization is sustained by Ih and INa,sub, and that delayed repolarizing feedback involves an IM-like current whose properties remain to be characterized. The multiple ionic mechanisms shown here to contribute to GoC pacemaking should provide the substrate for fine regulation of firing frequency and precision, thus influencing the cyclic inhibition exerted by GoCs onto the cerebellar GL.

Indexed as

Action PotentialsAnimalsBiological ClocksCells, CulturedCerebellumInterneuronsIon Channel GatingNerve NetPeriodicityRatsRats, WistarSodium ChannelsSodium Channels

Identifiers

PMID16690702
PMCPMC1817727
OpenAlexW1550335362

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.