Evidence map›Paper›PMID 18238813›Full record

ArticleThe Journal of physiology2008

Developmental changes in calcium/calmodulin-dependent inactivation of calcium currents at the rat calyx of Held.

Takeshi Nakamura, Takayuki Yamashita, Naoto Saitoh, Tomoyuki Takahashi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Activation of CaExperimental brain research · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Activity-dependent neurotrophin signaling underlies developmental switch of Ca2+ channel subtypes mediating neurotransmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  8. Theoretical models of synaptic short term plasticity.Frontiers in computational neuroscience · 2013
    Article
  9. Actin-dependent rapid recruitment of reluctant synaptic vesicles into a fast-releasing vesicle pool.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Interaction between facilitation and depression at a large CNS synapse reveals mechanisms of short-term plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  17. Article
  18. Synaptic vesicle pool size, release probability and synaptic depression are sensitive to Ca2+ buffering capacity in the developing rat calyx of Held.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2009
    Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

Takeshi NakamuraDoshisha University, Faculty of Life and Medical Sciences, Kyoto 619-0225, Japan.
Takayuki Yamashita
Naoto Saitoh
Tomoyuki Takahashi
Doshisha University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca2+-binding to calmodulin (CaM) causes facilitation and/or inactivation of recombinant Ca2+ channels. At the rat calyx of Held, before hearing onset, presynaptic Ca2+ currents (IpCa) undergo Ca2+/CaM-dependent inactivation during repetitive activation at around 1 Hz, implying that this may be a major cause of short-term synaptic depression. However, it remains open whether the Ca2+/CaM-dependent inactivation of IpCa persists in more mature animals. To address this question, we tested the effect of CaM inhibitors on the activity-dependent modulation of IpCa in calyces, before (postnatal day (P) 7-9) and after (P13-15) hearing onset. Our results indicate that the CaM-dependent IpCa inactivation during low-frequency stimulation, and the ensuing synaptic depression, occur only at calyces in the prehearing period. However, CaM immunoreactivity in P8 and P14 calyces was equally strong. Even at P13-15, high frequency stimulation (200-500 Hz) could induce IpCa inactivation, which was attenuated by EGTA (10 mM) or a CaM inhibitor peptide loaded into the terminal. Furthermore, the CaM inhibitor peptide attenuated a transient facilitation of IpCa preceding inactivation observed at 500 Hz stimulation, whereas it had no effect on sustained IpCa facilitations during trains of 50-200 Hz stimulation. These results suggest that the Ca2+/CaM-dependent IpCa modulation requires a high intraterminal Ca2+ concentration, which can be attained at immature calyces during low frequency stimulation, but only during unusually high frequency stimulation at calyceal terminals in the posthearing period.

Indexed as

AgingAnimalsBrain StemCalciumCalcium SignalingCalmodulinCells, CulturedEvoked Potentials, Auditory, Brain StemNeural InhibitionRatsRats, WistarCalciumCalmodulin

Identifiers

PMID18238813
PMCPMC2479563
OpenAlexW1537065123

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.