Evidence map›Paper›PMID 30421167›Full record

ArticleMolecular neurobiology2019

Involvement of the Cholinergic Parameters and Glial Cells in Learning Delay Induced by Glutaric Acid: Protection by N-Acetylcysteine.

Fernanda Silva Rodrigues, Viviane Nogueira de Zorzi, Marla Parizzi Funghetto, Fernanda Haupental, Alexandra Seide Cardoso, Sara Marchesan, Andréia M Cardoso, Maria Rosa C Schinger, Alencar Kolinski Machado, Ivana Beatrice Mânica da Cruz and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

17 authors at 3 institutions in 1 country.

Fernanda Silva RodriguesCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Viviane Nogueira de ZorziCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Marla Parizzi FunghettoCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Fernanda HaupentalCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Alexandra Seide CardosoCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Sara MarchesanCentro de Ciências Naturais e Exatas, Programa de Pós-graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Andréia M CardosoCentro de Ciências Naturais e Exatas, Programa de Pós-graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Maria Rosa C SchingerCentro de Ciências Naturais e Exatas, Programa de Pós-graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Alencar Kolinski MachadoCentro de Ciências da Saúde Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Ivana Beatrice Mânica da CruzCentro de Ciências da Saúde Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Marta Maria Medeiros Frescura DuarteCentro de Ciências da Saúde Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Léder L XavierFaculdade de Biociências, Laboratório Central de Microscopia e Microanálise, Departamento de Ciências Fisiológica, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, RS, 90610-000, Brazil.
Ana Flavia FurianCentro de Ciências da Saúde Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Mauro Schneider OliveiraCentro de Ciências da Saúde Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.
Adair Roberto Soares SantosCentro de Ciências Biológicas, Laboratório de Neurobiologia da Dor e Inflamação, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.
Luiz Fernando Freire RoyesCentro de Educação Física e Desportos, Departamento de Métodos e Técnicas Desportivas, Laboratório de Bioquímica do Exercício (BIOEX), Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Michele Rechia FigheraCentro de Ciências da Saúde, Departamento de Neuropsiquiatria, Laboratório de Neuropsiquiatria Experimental e Clínico, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil. mrfighera@yahoo.com.br.ORCID http://orcid.org/0000-0002-3111-7530
Universidade Federal de Santa Maria · BRPontifícia Universidade Católica do Rio Grande do Sul · BRUniversidade Federal de Santa Catarina · BR

Funding

LOCALIZATION AND REGULATION OF RENAL SODIUM CHANNELSF06TW002082 · FIC · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ERNST, STEPHEN A · 1994 to 1994
–
Conselho Nacional de Desenvolvimento Científico e Tecnológico 11/2082-4
6 · The paper itself

Abstract

Dysfunction of basal ganglia neurons is a characteristic of glutaric acidemia type I (GA-I), an autosomal recessive inherited neurometabolic disease characterized by deficiency of glutaryl-CoA dehydrogenase (GCDH) and accumulation of glutaric acid (GA). The affected patients present clinical manifestations such as motor dysfunction and memory impairment followed by extensive striatal neurodegeneration. Knowing that there is relevant striatal dysfunction in GA-I, the purpose of the present study was to verify the performance of young rats chronically injected with GA in working and procedural memory test, and whether N-acetylcysteine (NAC) would protect against impairment induced by GA. Rat pups were injected with GA (5 μmol g body weight

Indexed as

AcetylcysteineAnimalsCholinergic NeuronsGlutaratesMaleMaze LearningMemory DisordersNeurogliaRatsRats, WistarAcetylcysteineGlutaratesglutaric acidAcetylcholinesterase activityGlutaric acidInflammationMemoryN-acetylcysteineProcedural learningStriatumα7nAChR

Identifiers

PMID30421167
OpenAlexW2900833786

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.