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Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain

BACKGROUND: The anterior cingulate cortex (ACC) has been related to the affective component of pain. Dopaminergic mesocortical circuits, including the ACC, are able to inhibit neuropathic nociception measured as autotomy behaviour. We determined the changes in dopamine D1 and D2 (D1R and D2R) recept...

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Autores principales: Ortega-Legaspi, J Manuel, de Gortari, Patricia, Garduño-Gutiérrez, René, Amaya, María Isabel, León-Olea, Martha, Coffeen, Ulises, Pellicer, Francisco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3286425/
https://www.ncbi.nlm.nih.gov/pubmed/22171983
http://dx.doi.org/10.1186/1744-8069-7-97
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author Ortega-Legaspi, J Manuel
de Gortari, Patricia
Garduño-Gutiérrez, René
Amaya, María Isabel
León-Olea, Martha
Coffeen, Ulises
Pellicer, Francisco
author_facet Ortega-Legaspi, J Manuel
de Gortari, Patricia
Garduño-Gutiérrez, René
Amaya, María Isabel
León-Olea, Martha
Coffeen, Ulises
Pellicer, Francisco
author_sort Ortega-Legaspi, J Manuel
collection PubMed
description BACKGROUND: The anterior cingulate cortex (ACC) has been related to the affective component of pain. Dopaminergic mesocortical circuits, including the ACC, are able to inhibit neuropathic nociception measured as autotomy behaviour. We determined the changes in dopamine D1 and D2 (D1R and D2R) receptor expression in the ACC (cg1 and cg2) in an animal model of neuropathic pain. The neuropathic group had noxious heat applied in the right hind paw followed 30 min. later by right sciatic denervation. Autotomy score (AS) was recorded for eight days and subsequently classified in low, medium and high AS groups. The control consisted of naïve animals. A semiquantitative RT-PCR procedure was done to determine mRNA levels for D1R and D2R in cg1 and cg2, and protein levels were measured by Western Blot. RESULTS: The results of D1R mRNA in cg1 showed a decrease in all groups. D2R mRNA levels in cg1 decreased in low AS and increased in medium and high AS. Regarding D1R in cg2, there was an increase in all groups. D2R expression levels in cg2 decreased in all groups. In cg1, the D2R mRNA correlated positively with autotomy behaviour. Protein levels of D2R in cg1 increased in all groups but to a higher degree in low AS. In cg2 D2R protein only decreased discretely. D1R protein was not found in either ACC region. CONCLUSIONS: This is the first evidence of an increase of inhibitory dopaminergic receptor (D2R) mRNA and protein in cg1 in correlation with nociceptive behaviour in a neuropathic model of pain in the rat.
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spelling pubmed-32864252012-02-25 Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain Ortega-Legaspi, J Manuel de Gortari, Patricia Garduño-Gutiérrez, René Amaya, María Isabel León-Olea, Martha Coffeen, Ulises Pellicer, Francisco Mol Pain Research BACKGROUND: The anterior cingulate cortex (ACC) has been related to the affective component of pain. Dopaminergic mesocortical circuits, including the ACC, are able to inhibit neuropathic nociception measured as autotomy behaviour. We determined the changes in dopamine D1 and D2 (D1R and D2R) receptor expression in the ACC (cg1 and cg2) in an animal model of neuropathic pain. The neuropathic group had noxious heat applied in the right hind paw followed 30 min. later by right sciatic denervation. Autotomy score (AS) was recorded for eight days and subsequently classified in low, medium and high AS groups. The control consisted of naïve animals. A semiquantitative RT-PCR procedure was done to determine mRNA levels for D1R and D2R in cg1 and cg2, and protein levels were measured by Western Blot. RESULTS: The results of D1R mRNA in cg1 showed a decrease in all groups. D2R mRNA levels in cg1 decreased in low AS and increased in medium and high AS. Regarding D1R in cg2, there was an increase in all groups. D2R expression levels in cg2 decreased in all groups. In cg1, the D2R mRNA correlated positively with autotomy behaviour. Protein levels of D2R in cg1 increased in all groups but to a higher degree in low AS. In cg2 D2R protein only decreased discretely. D1R protein was not found in either ACC region. CONCLUSIONS: This is the first evidence of an increase of inhibitory dopaminergic receptor (D2R) mRNA and protein in cg1 in correlation with nociceptive behaviour in a neuropathic model of pain in the rat. BioMed Central 2011-12-15 /pmc/articles/PMC3286425/ /pubmed/22171983 http://dx.doi.org/10.1186/1744-8069-7-97 Text en Copyright ©2011 Ortega-Legaspi et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Ortega-Legaspi, J Manuel
de Gortari, Patricia
Garduño-Gutiérrez, René
Amaya, María Isabel
León-Olea, Martha
Coffeen, Ulises
Pellicer, Francisco
Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title_full Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title_fullStr Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title_full_unstemmed Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title_short Expression of the dopaminergic D1 and D2 receptors in the anterior cingulate cortex in a model of neuropathic pain
title_sort expression of the dopaminergic d1 and d2 receptors in the anterior cingulate cortex in a model of neuropathic pain
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3286425/
https://www.ncbi.nlm.nih.gov/pubmed/22171983
http://dx.doi.org/10.1186/1744-8069-7-97
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