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

Fiona E Holmes; Niall C H Kerr; Penny A Vanderplank; Craig McArdle; David Wynick

doi:10.1016/j.mcn.2016.11.010

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

Fiona E Holmes, Niall C H Kerr, Penny A Vanderplank, Craig McArdle, David Wynick^*

^*Corresponding author for this work

Research output: Contribution to journal › Article (Academic Journal) › peer-review

17 Citations (Scopus)

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Abstract

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.

Original language	English
Pages (from-to)	35-40
Number of pages	6
Journal	Molecular and Cellular Neuroscience
Volume	78
Early online date	30 Nov 2016
DOIs	https://doi.org/10.1016/j.mcn.2016.11.010
Publication status	Published - 1 Jan 2017

Bibliographical note

28 November 2016

Keywords

Dorsal root ganglion
Galanin
GalR1
GalR2
Gpr151
Pain

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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",

abstract = "BackgroundGpr151 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.ResultsReal-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.ConclusionsOur 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.",

keywords = "Dorsal root ganglion, Galanin, GalR1, GalR2, Gpr151, Pain",

author = "Holmes, {Fiona E} and Kerr, {Niall C H} and Vanderplank, {Penny A} and Craig McArdle and David Wynick",

note = "28 November 2016",

year = "2017",

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doi = "10.1016/j.mcn.2016.11.010",

language = "English",

volume = "78",

pages = "35--40",

journal = "Molecular and Cellular Neuroscience",

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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. / Holmes, Fiona E; Kerr, Niall C H; Vanderplank, Penny A et al.
In: Molecular and Cellular Neuroscience, Vol. 78, 01.01.2017, p. 35-40.

Research output: Contribution to journal › Article (Academic Journal) › peer-review

TY - JOUR

T1 - 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

AU - Holmes, Fiona E

AU - Kerr, Niall C H

AU - Vanderplank, Penny A

AU - McArdle, Craig

AU - Wynick, David

N1 - 28 November 2016

PY - 2017/1/1

Y1 - 2017/1/1

N2 - BackgroundGpr151 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.ResultsReal-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.ConclusionsOur 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.

AB - BackgroundGpr151 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.ResultsReal-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.ConclusionsOur 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.

KW - Dorsal root ganglion

KW - Galanin

KW - GalR1

KW - GalR2

KW - Gpr151

KW - Pain

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DO - 10.1016/j.mcn.2016.11.010

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SN - 1044-7431

VL - 78

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JO - Molecular and Cellular Neuroscience

JF - Molecular and Cellular Neuroscience

ER -

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

Abstract

Bibliographical note

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THE ROLE OF GALANIN IN THE ADAPTIVE RESPONSE OF THE PERIPHERAL NERVOUS SYSTEMT O INJURY

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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

Abstract

Bibliographical note

Keywords

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