Evidence map›Paper›PMID 20810905›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

P/Q and N channels control baseline and spike-triggered calcium levels in neocortical axons and synaptic boutons.

Yuguo Yu, Carlos Maureira, Xiuxin Liu, David McCormick

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  11. CDK5/p35-Dependent Microtubule Reorganization Contributes to Homeostatic Shortening of the Axon Initial Segment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Functional Microstructure of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  13. Article
  14. Article
  15. CaeLife · 2020
    Article
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  17. Review
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  19. KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
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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 1 institution in 1 country.

Yuguo YuDepartment of Neurobiology, Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Carlos Maureira
Xiuxin Liu
David McCormick
Yale University · US

Funding

Neurotransmitter Actions in Neocortex and ThalamusR37NS026143 · NINDS · YALE UNIVERSITY · PI MCCORMICK, DAVID · 2005 to 2011
$3.0M
Properties of Axons and Synaptic Communication in the NeocortexR01NS060135 · NINDS · YALE UNIVERSITY · PI MCCORMICK, DAVID · 2008 to 2011
$2.0M
NINDS NIH HHS R01 NS060135NINDS NIH HHS R37 NS026143
6 · The paper itself

Abstract

Cortical axons contain a diverse range of voltage-activated ion channels, including Ca(2+) currents. Interestingly, Ca(2+) channels are not only located at presynaptic terminals, but also in the axon initial segment (AIS), suggesting a potentially important role in the regulation of action potential generation and neuronal excitability. Here, using two-photon microscopy and whole-cell patch-clamp recording, we examined the properties and role of calcium channels located in the AIS and presynaptic terminals of ferret layer 5 prefrontal cortical pyramidal cells in vitro. Subthreshold depolarization of the soma resulted in an increase in baseline and spike-triggered calcium concentration in both the AIS and nearby synaptic terminals. The increase in baseline calcium concentration rose with depolarization and fell with hyperpolarization with a time constant of approximately 1 s and was blocked by removal of Ca(2+) from the bathing medium. The increases in calcium concentration at the AIS evoked by subthreshold or suprathreshold depolarization of the soma were blocked by the P/Q-channel antagonist omega-agatoxin IVA or the N-channel antagonist omega-conotoxin GVIA or both. The presence of these channels in the AIS pyramidal cells was confirmed with immunochemistry. Block of these channels slowed axonal action potential repolarization, apparently from reduction of the activation of a Ca(2+)-activated K(+) current, and increased neuronal excitability. These results demonstrate novel mechanisms by which calcium currents may control the electrophysiological properties of axonal spike generation and neurotransmitter release in the neocortex.

Indexed as

Action PotentialsAnimalsAxonsCalciumCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCalcium SignalingFemaleFerretsMaleNeocortexPresynaptic TerminalsCalciumCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-Type

Identifiers

PMID20810905
PMCPMC2947942
OpenAlexW2021951036

What OpenQuestion holds

Textmetadata
LicenceTDM
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.