Evidence map›Paper›PMID 39105899›Full record

ArticleNeurochemical research2024

Changes in Noradrenergic Synthesis and Dopamine Beta-Hydroxylase Activity in Response to Oxidative Stress after Iron-induced Brain Injury.

Antonio Verduzco-Mendoza, Daniel Mota-Rojas, Adriana Olmos-Hernández, Alberto Avila-Luna, Karla García-García, Arturo Gálvez-Rosas, Alberto Hidalgo-Bravo, Camilo Ríos, Carmen Parra-Cid, Sergio Montes and 5 more

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Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

15 authors.

Antonio Verduzco-MendozaPrograma de Doctorado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Ciudad de México, Mexico.
Daniel Mota-RojasDivisión de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana CBS, Unidad Xochimilco, Ciudad de México, Mexico.
Adriana Olmos-HernándezDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Alberto Avila-LunaDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Karla García-GarcíaDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Arturo Gálvez-RosasDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Alberto Hidalgo-BravoDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Camilo RíosDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Carmen Parra-CidDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Sergio MontesUnidad Académica Multidisciplinaria Reynosa-Aztlán, Universidad Autónoma de Tamaulipas, calle 16 y lago de Chapala, Aztlán, Tamaulipas, Mexico.
Julieta García-LópezDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico.
Laura E Ramos-LangurenFacultad de Psicología, División de Estudios Profesionales, Universidad Nacional Autónoma de Mexico, Av. Universidad 3040, Col, Copilco Universidad Alcaldía Coyoacán, Ciudad de México, Mexico.
Francisca Pérez-SeverianoLaboratorio de Neurofarmacología Molecular y Nanotecnología, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, SSa, Insurgentes Sur 3877, Ciudad de México, Mexico.
Rigoberto González-PiñaSección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Salvador Díaz Mirón esq. Plan de San Luis S/N, Miguel Hidalgo, Casco de Santo Tomas, 11340, Ciudad de México, Mexico.
Antonio Bueno-NavaDirección de Investigación, Arenal de Guadalupe, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calzada México-Xochimilco 289, Arenal de Guadalupe, Ciudad de México, Mexico. abueno@inr.gob.mx.

Funding

Consejo Nacional de Ciencia y Tecnología CB-2016-287614Consejo Nacional de Ciencia y Tecnología CB-2016-288512
6 · The paper itself

Abstract

Noradrenaline (NA) levels are altered during the first hours and several days after cortical injury. NA modulates motor functional recovery. The present study investigated whether iron-induced cortical injury modulated noradrenergic synthesis and dopamine beta-hydroxylase (DBH) activity in response to oxidative stress in the brain cortex, pons and cerebellum of the rat. Seventy-eight rats were divided into two groups: (a) the sham group, which received an intracortical injection of a vehicle solution; and (b) the injured group, which received an intracortical injection of ferrous chloride. Motor deficits were evaluated for 20 days post-injury. On the 3rd and 20th days, the rats were euthanized to measure oxidative stress indicators (reactive oxygen species (ROS), reduced glutathione (GSH) and oxidized glutathione (GSSG)) and catecholamines (NA, dopamine (DA)), plus DBH mRNA and protein levels. Our results showed that iron-induced brain cortex injury increased noradrenergic synthesis and DBH activity in the brain cortex, pons and cerebellum at 3 days post-injury, predominantly on the ipsilateral side to the injury, in response to oxidative stress. A compensatory increase in contralateral noradrenergic activity was observed, but without changes in the DBH mRNA and protein levels in the cerebellum and pons. In conclusion, iron-induced cortical injury increased the noradrenergic response in the brain cortex, pons and cerebellum, particularly on the ipsilateral side, accompanied by a compensatory response on the contralateral side. The oxidative stress was countered by antioxidant activity, which favored functional recovery following motor deficits.

Indexed as

Brain InjuriesDopamine beta-HydroxylaseNorepinephrineOxidative StressAnimalsFerrous CompoundsIronMaleRatsRats, WistarReactive Oxygen SpeciesDopamine beta-Hydroxylaseferrous chlorideFerrous CompoundsIronNorepinephrineReactive Oxygen SpeciesDopamine beta hydroxylase (DBH)Dopamine (DA)Motor functional recoveryNoradrenergic activityOxidative stressOxidized glutathione (GSSG)Reactive oxygen species (ROS)Reduced glutathione (GSH)

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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.