Evidence map›Paper›PMID 24133278›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Glycine transporter-1 inhibition promotes striatal axon sprouting via NMDA receptors in dopamine neurons.

Yvonne Schmitz, Candace Castagna, Ana Mrejeru, José E Lizardi-Ortiz, Zoe Klein, Craig W Lindsley, David Sulzer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. GlyT1 (SLC6A9) inhibition in neurological and psychiatric disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. [Experimental brain research · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. VGluT2 Expression in Dopamine Neurons Contributes to Postlesional Striatal Reinnervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  12. Review
  13. Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016
    Review
  14. Review
  15. The multilingual nature of dopamine neurons.Progress in brain research · 2014
    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

7 authors at 2 institutions in 1 country.

Yvonne SchmitzDepartments of Neurology, Psychiatry, and Pharmacology, Columbia University Medical Center, New York, New York 10032, and Vanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Candace Castagna
Ana Mrejeru
José E Lizardi-Ortiz
Zoe Klein
Craig W Lindsley
David Sulzer
Columbia University Irving Medical Center · USVanderbilt University Medical Center · 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

NMDA receptor activity is involved in shaping synaptic connections throughout development and adulthood. We recently reported that brief activation of NMDA receptors on cultured ventral midbrain dopamine neurons enhanced their axon growth rate and induced axonal branching. To test whether this mechanism was relevant to axon regrowth in adult animals, we examined the reinnervation of dorsal striatum following nigral dopamine neuron loss induced by unilateral intrastriatal injections of the toxin 6-hydroxydopamine. We used a pharmacological approach to enhance NMDA receptor-dependent signaling by treatment with an inhibitor of glycine transporter-1 that elevates levels of extracellular glycine, a coagonist required for NMDA receptor activation. All mice displayed sprouting of dopaminergic axons from spared fibers in the ventral striatum to the denervated dorsal striatum at 7 weeks post-lesion, but the reinnervation in mice treated for 4 weeks with glycine uptake inhibitor was approximately twice as dense as in untreated mice. The treated mice also displayed higher levels of striatal dopamine and a complete recovery from lateralization in a test of sensorimotor behavior. We confirmed that the actions of glycine uptake inhibition on reinnervation and behavioral recovery required NMDA receptors in dopamine neurons using targeted deletion of the NR1 NMDA receptor subunit in dopamine neurons. Glycine transport inhibitors promote functionally relevant sprouting of surviving dopamine axons and could provide clinical treatment for disorders such as Parkinson's disease.

Indexed as

AnimalsAxonsBehavior, AnimalCorpus StriatumDopaminergic NeuronsGlycine Plasma Membrane Transport ProteinsMesencephalonMiceMotor SkillsOxidopamineParkinson Disease, SecondaryReceptors, N-Methyl-D-AspartateRecovery of FunctionSubstantia NigraGlycine Plasma Membrane Transport ProteinsOxidopamineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID24133278
PMCPMC3797382
OpenAlexW2036176553

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.