Evidence map›Paper›PMID 19776283›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Glutamate controls growth rate and branching of dopaminergic axons.

Yvonne Schmitz, James Luccarelli, Minji Kim, Mi Wang, David Sulzer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Possible Mechanisms of Tau Spread and Toxicity in Alzheimer's Disease.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. VGluT2 Expression in Dopamine Neurons Contributes to Postlesional Striatal Reinnervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016
    Review
  16. Article
  17. Article
  18. Article
  19. Premyelinated central axons express neurotoxic NMDA receptors: relevance to early developing white-matter injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  20. 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

5 authors at 3 institutions in 1 country.

Yvonne SchmitzDepartments of Neurology, Columbia University School of Medicine, New York State Psychiatric Institute, New York, 10032, USA. ys290@columbia.edu
James Luccarelli
Minji Kim
Mi Wang
David Sulzer
Columbia University · USNew York Psychoanalytic Society and Institute · USUniversity School · US

Funding

The Dopamine Synapse and Associative LearningR01DA007418 · NIDA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David Sulzer · 1999 to 2026
$9.4M
NIDA NIH HHS R01 DA007418
6 · The paper itself

Abstract

Dopamine-releasing neurons of the substantia nigra pars compacta produce an extraordinarily dense and expansive plexus of innervation in the striatum converging with glutamatergic corticostriatal and thalamostriatal axon terminals at dendritic spines of medium spiny neurons. Here, we investigated whether glutamatergic signaling promotes arborization and growth of dopaminergic axons. In postnatal ventral midbrain cultures, dopaminergic axons rapidly responded to glutamate stimulation with accelerated growth and growth cone splitting when NMDA and AMPA/kainate receptors were activated. In contrast, when AMPA/kainate receptors were selectively activated, axon growth rate was decreased. To address whether this switch in axonal growth response was mediated by distinct calcium signals, we used calcium imaging. Combined NMDA and AMPA/kainate receptor activation elicited calcium signals in axonal growth cones that were mediated by calcium influx through L-type voltage-gated calcium channels and ryanodine receptor-induced calcium release from intracellular stores. AMPA/kainate receptor activation alone elicited calcium signals that were solely attributable to calcium influx through L-type calcium channels. We found that inhibitors of calcium/calmodulin-dependent protein kinases prevented the NMDA receptor-dependent axonal growth acceleration, whereas AMPA/kainate-induced axonal growth decrease was blocked by inhibitors of calcineurin and by increased cAMP levels. Our data suggest that the balance between NMDA and AMPA/kainate receptor activation regulates the axonal arborization pattern of dopamine axons through the activation of competing calcium-dependent signaling pathways. Understanding the mechanisms of dopaminergic axonal arborization is essential to the development of treatments that aim to restore dopaminergic innervation in Parkinson's disease.

Indexed as

alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsAxonsCalcineurin InhibitorsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium Channels, L-TypeCells, CulturedCyclic AMPDopamineGlutamic AcidGrowth ConesIntracellular SpaceKainic AcidKainic Acid ReceptorsMesencephalonalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidCalcineurin InhibitorsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium Channels, L-TypeCyclic AMPDopamineGlutamic AcidKainic AcidKainic Acid ReceptorsReceptors, AMPAReceptors, N-Methyl-D-AspartateRyanodine Receptor Calcium Release Channel

Identifiers

PMID19776283
PMCPMC2818361
OpenAlexW2030069437

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.