Evidence map›Paper›PMID 20357104›Full record

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

Different relationship of N- and P/Q-type Ca2+ channels to channel-interacting slots in controlling neurotransmission at cultured hippocampal synapses.

Yu-Qing Cao, Richard W Tsien

Abstract read
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 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

  1. Article
  2. Review
  3. Nanoarchitecture of CaBrain pathology (Zurich, Switzerland) · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Targeting mitochondrial CaThe Journal of physiology · 2024
    Review
  8. Physiologic and Nanoscale Distinctions Define Glutamatergic Synapses in Tonic vs Phasic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Article
  10. Article
  11. Involvement of CaThe Journal of physiology · 2022
    Article
  12. Article
  13. Single Calcium Channel Nanodomains Drive Presynaptic Calcium Entry at Lamprey Reticulospinal Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Primary and secondary motoneurons use different calcium channel types to control escape and swimming behaviors in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    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

2 authors.

Yu-Qing CaoDepartment of Molecular and Cellular Physiology, Beckman Center, Stanford University School of Medicine, Stanford, California 94305-5345, USA.
Richard W Tsien

Funding

NEURONAL FUNCTIONS OF MULTIPLE TYPES OF CALCIUM CHANNELSR01NS024067 · NINDS · YALE UNIVERSITY · PI TSIEN, RICHARD W · 1986 to 2014
$5.0M
NINDS NIH HHS NS24067NINDS NIH HHS R01 NS024067
6 · The paper itself

Abstract

Synaptic transmission at CNS synapses is often mediated by joint actions of multiple Ca(2+) channel subtypes, most prominently, P/Q- and N-type. We have proposed that P/Q-type Ca(2+) channels saturate type-preferring slots at presynaptic terminals, which impose a ceiling on the synaptic efficacy of the channels. To test for analogous interactions for presynaptic N-type Ca(2+) channels, we overexpressed their pore-forming Ca(V)2.2 subunit in cultured mouse hippocampal neurons, recorded excitatory synaptic transmission from transfected cells, and dissected the contributions of N-, P/Q-, and R-type channels with subtype-specific blockers. Overexpression of Ca(V)2.2 did not increase the absolute size of the EPSC even though somatic N-type current was augmented by severalfold. Thus, the strength of neurotransmission is saturated with regard to levels of Ca(2+) channel expression for both N-type and P/Q-type channels. Overexpression of Ca(2+)-impermeable Ca(V)2.2 subunits decreased EPSC size, corroborating competition for channel slots. Striking asymmetries between N- and P/Q-type channels emerged when their relative contributions were compared with channel overexpression. Overexpressed N-type channels could competitively displace P/Q-type channels from P/Q-preferring slots and take over the role of supporting transmission. The converse was not found with overexpression of P/Q-type channels, regardless of their C-terminal domain. We interpret these findings in terms of two different kinds of presynaptic slots at excitatory synapses, one accepting N-type channels but rejecting P/Q-type (N(specific)) and the other preferring P/Q-type but also accepting N-type (PQ(preferring)). The interaction between channels and slots governs the respective contributions of multiple channel types to neurotransmission and, in turn, the ability of transmission to respond to various stimulus patterns and neuromodulators.

Indexed as

Action PotentialsAnimalsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCells, CulturedHippocampusHumansMiceNeuronsPatch-Clamp TechniquesProtein IsoformsProtein SubunitsSynapsesSynaptic TransmissionCACNA1B protein, humanCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeProtein IsoformsProtein Subunits

Identifiers

PMID20357104
PMCPMC3842455

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.