Evidence map›Paper›PMID 24285882›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Activity-dependent neurotrophin signaling underlies developmental switch of Ca2+ channel subtypes mediating neurotransmitter release.

Takafumi Miki, Hirokazu Hirai, Tomoyuki Takahashi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  2. Involvement of CaThe Journal of physiology · 2022
    Article
  3. Review
  4. CaNeuron · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. C-terminal splice variants of P/Q-type CaThe Journal of biological chemistry · 2017
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Strength and precision of neurotransmission at mammalian presynaptic terminals.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2015
    Review
  19. The role for alterations in neuronal activity in the pathogenesis of polyglutamine repeat disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014
    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

3 authors at 3 institutions in 1 country.

Takafumi MikiLaboratory of Molecular Synaptic Function, Doshisha University Graduate School of Brain Science, Kyotanabe 610-0394, Japan, Department of Neurophysiology, Gunma University Graduate School of Medicine, Gunma 371-8511, Japan, and Celluar and Molecular Synaptic Function Unit, Okinawa Institute of Science and Technology Graduate University (OIST), Okinawa 904-0495, Japan.
Hirokazu Hirai
Tomoyuki Takahashi
Doshisha University · JPGunma University · JPOkinawa Institute of Science and Technology Graduate University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At the nerve terminal, neurotransmitter release is triggered by Ca(2+) influx through voltage-gated Ca(2+) channels (VGCCs). During postnatal development, VGCC subtypes in the nerve terminal switch at many synapses. In immature rodent cerebella, N-type and P/Q-type VGCCs mediate GABAergic neurotransmission from Purkinje cells (PCs) to deep nuclear cells, but as animals mature, neurotransmission becomes entirely P/Q-type dependent. We reproduced this developmental switch in rat cerebellar slice culture to address the underlying mechanism. Chronic block of cerebellar neuronal activity with tetrodotoxin (TTX) in slice culture, or in vivo, reversed the switch, leaving neurotransmission predominantly N-type channel-dependent. Brain-derived neurotrophic factor or neurotrophin-4 rescued this TTX effect, whereas pharmacological blockade of neurotrophin receptors mimicked the TTX effect. In PC somata, unlike in presynaptic terminals, TTX had no effect on the proportion of Ca(2+) channel subtype currents. We conclude that neuronal activity activates the neurotrophin-TrkB signaling pathway, thereby causing the N-to-P/Q channel switch in presynaptic terminals.

Indexed as

Anesthetics, LocalAnimalsBrain-Derived Neurotrophic FactorCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCerebellumElectrophysiological PhenomenaFemaleGenetic VectorsImmunohistochemistryIn Vitro TechniquesLentivirusMaleNerve EndingsAnesthetics, LocalBrain-Derived Neurotrophic FactorCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeNerve Growth FactorsNeurotransmitter AgentsReceptor, trkBTetrodotoxin

Identifiers

PMID24285882
PMCPMC6618703
OpenAlexW1993394492

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.