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Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain
BACKGROUND: Gpr151 is an orphan GPCR whose function is unknown. The restricted pattern of neuronal expression in the habenula, dorsal horn of the spinal cord and dorsal root ganglion plus homology with the galanin family of receptors imply a role in nociception. RESULTS: Real-time quantitative RT-PC...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Academic Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5235321/ https://www.ncbi.nlm.nih.gov/pubmed/27913310 http://dx.doi.org/10.1016/j.mcn.2016.11.010 |
_version_ | 1782495138809905152 |
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author | Holmes, Fiona E. Kerr, Niall Chen, Ying-Ju Vanderplank, Penny McArdle, Craig A. Wynick, David |
author_facet | Holmes, Fiona E. Kerr, Niall Chen, Ying-Ju Vanderplank, Penny McArdle, Craig A. Wynick, David |
author_sort | Holmes, Fiona E. |
collection | PubMed |
description | BACKGROUND: Gpr151 is an orphan GPCR whose function is unknown. The restricted pattern of neuronal expression in the habenula, dorsal horn of the spinal cord and dorsal root ganglion plus homology with the galanin family of receptors imply a role in nociception. RESULTS: Real-time quantitative RT-PCR demonstrated a 49.9 ± 2.9 fold highly significant (P < 0.001) increase in Gpr151 mRNA expression in the dorsal root ganglion 7 days after the spared nerve injury model of neuropathic pain. Measures of acute, inflammatory and neuropathic pain behaviours were not significantly different using separate groups of Gpr151 loss-of-function mutant mice and wild-type controls. Galanin at concentrations between 100 nM and 10 μM did not induce calcium signalling responses in ND7/23 cells transfected with Gpr151. CONCLUSIONS: Our results indicate that despite the very large upregulation in the DRG after a nerve injury model of neuropathic pain, the Gpr151 orphan receptor does not appear to be involved in the modulation of pain-related behaviours. Further, galanin is unlikely to be an endogenous ligand for Gpr151. |
format | Online Article Text |
id | pubmed-5235321 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Academic Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-52353212017-01-23 Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain Holmes, Fiona E. Kerr, Niall Chen, Ying-Ju Vanderplank, Penny McArdle, Craig A. Wynick, David Mol Cell Neurosci Article BACKGROUND: Gpr151 is an orphan GPCR whose function is unknown. The restricted pattern of neuronal expression in the habenula, dorsal horn of the spinal cord and dorsal root ganglion plus homology with the galanin family of receptors imply a role in nociception. RESULTS: Real-time quantitative RT-PCR demonstrated a 49.9 ± 2.9 fold highly significant (P < 0.001) increase in Gpr151 mRNA expression in the dorsal root ganglion 7 days after the spared nerve injury model of neuropathic pain. Measures of acute, inflammatory and neuropathic pain behaviours were not significantly different using separate groups of Gpr151 loss-of-function mutant mice and wild-type controls. Galanin at concentrations between 100 nM and 10 μM did not induce calcium signalling responses in ND7/23 cells transfected with Gpr151. CONCLUSIONS: Our results indicate that despite the very large upregulation in the DRG after a nerve injury model of neuropathic pain, the Gpr151 orphan receptor does not appear to be involved in the modulation of pain-related behaviours. Further, galanin is unlikely to be an endogenous ligand for Gpr151. Academic Press 2017-01 /pmc/articles/PMC5235321/ /pubmed/27913310 http://dx.doi.org/10.1016/j.mcn.2016.11.010 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Holmes, Fiona E. Kerr, Niall Chen, Ying-Ju Vanderplank, Penny McArdle, Craig A. Wynick, David Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title | Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title_full | Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title_fullStr | Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title_full_unstemmed | Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title_short | Targeted disruption of the orphan receptor Gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
title_sort | targeted disruption of the orphan receptor gpr151 does not alter pain-related behaviour despite a strong induction in dorsal root ganglion expression in a model of neuropathic pain |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5235321/ https://www.ncbi.nlm.nih.gov/pubmed/27913310 http://dx.doi.org/10.1016/j.mcn.2016.11.010 |
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