Evidence map›Paper›PMID 18957221›Full record

ArticleNeuron2008

Dendritic NMDA receptors activate axonal calcium channels.

Jason M Christie, Craig E Jahr

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2008. 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
3.7field-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

54 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. GluN2A- and GluN2B-containing pre-synapticPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  5. Article
  6. Article
  7. Synaptic NMDA receptor activity at resting membrane potentials.Frontiers in cellular neuroscience · 2022
    Article
  8. Article
  9. Neuropilin 2 Signaling Mediates Corticostriatal Transmission, Spine Maintenance, and Goal-Directed Learning in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Granular Layer Neurons Control Cerebellar Neurovascular Coupling Through an NMDA Receptor/NO-Dependent System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  14. Article
  15. Neuroligins Are Selectively Essential for NMDAR Signaling in Cerebellar Stellate Interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Excitation by Axon Terminal GABA Spillover in a Sound Localization Circuit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
  18. Review
  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

2 authors at 2 institutions in 1 country.

Jason M ChristieVollum Institute, Oregon Health & Science University, Portland, OR 97239-3098, USA. christij@ohsu.edu
Craig E Jahr
Oregon Health & Science University · USVollum Institute · US

Funding

GLUTAMATE RELEASE AND UPTAKE AT CEREBELLAR SYNAPSESR01NS040056 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI JAHR, CRAIG E · 2000 to 2014
$3.6M
Glutamate release and uptake at central synapsesR56NS040056 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI JAHR, CRAIG E · 2010 to 2010
$385k
NINDS NIH HHS NS40056NINDS NIH HHS R01 NS040056NINDS NIH HHS R56 NS040056
6 · The paper itself

Abstract

NMDA receptor (NMDAR) activation can alter synaptic strength by regulating transmitter release from a variety of neurons in the CNS. As NMDARs are permeable to Ca(2+) and monovalent cations, they could alter release directly by increasing presynaptic Ca(2+) or indirectly by axonal depolarization sufficient to activate voltage-sensitive Ca(2+) channels (VSCCs). Using two-photon microscopy to measure Ca(2+) excursions, we found that somatic depolarization or focal activation of dendritic NMDARs elicited small Ca(2+) transients in axon varicosities of cerebellar stellate cell interneurons. These axonal transients resulted from Ca(2+) entry through VSCCs that were opened by the electrotonic spread of the NMDAR-mediated depolarization elicited in the dendrites. In contrast, we were unable to detect direct activation of NMDARs on axons, indicating an exclusive somatodendritic expression of functional NMDARs. In cerebellar stellate cells, dendritic NMDAR activation masquerades as a presynaptic phenomenon and may influence Ca(2+) -dependent forms of presynaptic plasticity and release.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingCerebellar CortexDendritesExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsGlutamic AcidInterneuronsIon Channel GatingLong-Term Synaptic DepressionMembrane PotentialsMicroscopy, ConfocalOrgan Culture TechniquesPatch-Clamp TechniquesCalciumCalcium ChannelsExcitatory Amino Acid AgonistsGlutamic AcidReceptors, N-Methyl-D-Aspartate

Identifiers

PMID18957221
PMCPMC2644657
OpenAlexW2024312922

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.