Evidence map›Paper›PMID 26966009›Full record

ArticleNeurotoxicity research2016

L-DOPA Reverses the Increased Free Amino Acids Tissue Levels Induced by Dopamine Depletion and Rises GABA and Tyrosine in the Striatum.

Oscar Solís, Patricia García-Sanz, Antonio S Herranz, María-José Asensio, Rosario Moratalla

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Astrocytes modulate extracellular neurotransmitter levels and excitatory neurotransmission in dorsolateral striatum via dopamine D2 receptor signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Dopamine receptors: homomeric and heteromeric complexes in L-DOPA-induced dyskinesia.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  9. Article
  10. Levodopa treatment and dendritic spine pathology.Movement disorders : official journal of the Movement Disorder Society · 2018
    Review
  11. Article
  12. Review
  13. Article
  14. 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

5 authors at 4 institutions in 1 country.

Oscar SolísInstituto Cajal, CSIC, Av. Dr. Arce 37, 28002, Madrid, Spain.
Patricia García-SanzInstituto Cajal, CSIC, Av. Dr. Arce 37, 28002, Madrid, Spain.
Antonio S HerranzServicio Neurobiología, Hospital Universitario Ramón y Cajal, IRYCIS, 28034, Madrid, Spain.
María-José AsensioServicio Neurobiología, Hospital Universitario Ramón y Cajal, IRYCIS, 28034, Madrid, Spain.
Rosario MoratallaInstituto Cajal, CSIC, Av. Dr. Arce 37, 28002, Madrid, Spain. moratalla@cajal.csic.es.
Biomedical Research Networking Center on Neurodegenerative Diseases · ESHospital Universitario Ramón y Cajal · ESInstituto de Salud Carlos III · ESInstituto Ramón y Cajal de Investigación Sanitaria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perturbations in the cerebral levels of various amino acids are associated with neurological disorders, and previous studies have suggested that such alterations have a role in the motor and non-motor symptoms of Parkinson's disease. However, the direct effects of chronic L-DOPA treatment, that produces dyskinesia, on neural tissue amino acid concentrations have not been explored in detail. To evaluate whether striatal amino acid concentrations are altered in peak dose dyskinesia, 6-hydroxydopamine (6-OHDA)-lesioned hemiparkinsonian mice were treated chronically with L-DOPA and tissue amino acid concentrations were assessed by HPLC analysis. These experiments revealed that neither 6-OHDA nor L-DOPA treatment are able to alter glutamate in the striatum. However, glutamine increases after 6-OHDA and returns back to normal levels with L-DOPA treatment, suggesting increased striatal glutamatergic transmission with lack of dopamine. In addition, glycine and taurine levels are increased following dopamine denervation and restored to normal levels by L-DOPA. Interestingly, dyskinetic animals showed increased levels of GABA and tyrosine, while aspartate striatal tissue levels are not altered. Overall, our results indicate that chronic L-DOPA treatment, besides normalizing the altered levels of some amino acids after 6-OHDA, robustly increases striatal GABA and tyrosine levels which may in turn contribute to the development of L-DOPA-induced dyskinesia.

Indexed as

Amino AcidsAnimalsAspartic AcidCorpus StriatumDopamineDyskinesia, Drug-InducedForelimbgamma-Aminobutyric AcidGlutamic AcidGlycineLevodopaMiceOxidopamineRotarod Performance TestTaurineTyrosineAmino AcidsAspartic AcidDopaminegamma-Aminobutyric AcidGlutamic AcidGlycineLevodopaOxidopamineTaurineTyrosineAbnormal involuntary movementsGABAGlutamateGlutamineGlycineParkinson’s diseaseTaurineTyrosine

Identifiers

PMID26966009
OpenAlexW2294301440

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.