Evidence map›Paper›PMID 27063549›Full record

ArticleScientific reports2016

Neural ablation of the PARK10 candidate Plpp3 leads to dopaminergic transmission deficits without neurodegeneration.

Sandra Gómez-López, Ana Valeria Martínez-Silva, Teresa Montiel, Daniel Osorio-Gómez, Federico Bermúdez-Rattoni, Lourdes Massieu, Diana Escalante-Alcalde

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  5. Endothelial S1PCirculation research · 2021
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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 1 institution in 1 country.

Sandra Gómez-LópezInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Ana Valeria Martínez-SilvaInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Teresa MontielInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Daniel Osorio-GómezInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Federico Bermúdez-RattoniInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Lourdes MassieuInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Diana Escalante-AlcaldeInstituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México, Circuito Exterior s/n, Ciudad Universitaria, Mexico City, 04510, Mexico.
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a multifactorial neurodegenerative disorder, characterised by the progressive loss of midbrain dopaminergic neurons and a variety of motor symptoms. The gene coding for the phospholipid phosphatase 3, PLPP3 (formerly PPAP2B or LPP3), maps within the PARK10 locus, a region that has been linked with increased risk to late-onset PD. PLPP3 modulates the levels of a range of bioactive lipids controlling fundamental cellular processes within the central nervous system. Here we show that PLPP3 is enriched in astroglial cells of the adult murine ventral midbrain. Conditional inactivation of Plpp3 using a Nestin::Cre driver results in reduced mesencephalic levels of sphingosine-1-phosphate receptor 1 (S1P1), a well-known mediator of pro-survival responses. Yet, adult PLPP3-deficient mice exhibited no alterations in the number of dopaminergic neurons or in the basal levels of striatal extracellular dopamine (DA). Potassium-evoked DA overflow in the striatum, however, was significantly decreased in mutant mice. Locomotor evaluation revealed that, although PLPP3-deficient mice exhibit motor impairment, this is not progressive or responsive to acute L-DOPA therapy. These findings suggest that disruption of Plpp3 during early neural development leads to dopaminergic transmission deficits in the absence of nigrostriatal degeneration, and without causing an age-related locomotor decline consistent with PD.

Indexed as

AnimalsDisease Models, AnimalDopamineDopaminergic NeuronsFemaleGenetic LociLocomotionMesencephalonMiceMice, KnockoutMice, TransgenicMicroscopy, FluorescenceParkinson DiseasePhospholipid Transfer ProteinsProprotein ConvertasesSerine EndopeptidasesDopaminemembrane-bound transcription factor peptidase, site 1Phospholipid Transfer ProteinsPlscr3 protein, mouseProprotein ConvertasesSerine Endopeptidases

Identifiers

PMID27063549
PMCPMC4827058
OpenAlexW2329494663

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.