Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice

Abstract The G-protein coupled receptor GPR55 has been postulated to serve as a novel cannabinoid receptor. A previous report indicated that GPR55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR55 in the control of nociceptive responding. However, GPR...

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Autores principales:	Lawrence M. Carey, Tannia Gutierrez, Liting Deng, Wan-Hung Lee, Ken Mackie, Andrea G. Hohmann
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4b5b7f6227954b9f86d12bdebdc63a59
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spelling	oai:doaj.org-article:4b5b7f6227954b9f86d12bdebdc63a592021-12-02T15:05:58ZInflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice10.1038/s41598-017-01062-22045-2322https://doaj.org/article/4b5b7f6227954b9f86d12bdebdc63a592017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01062-2https://doaj.org/toc/2045-2322Abstract The G-protein coupled receptor GPR55 has been postulated to serve as a novel cannabinoid receptor. A previous report indicated that GPR55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR55 in the control of nociceptive responding. However, GPR55 knockout mice remain incompletely characterized in models of pathological pain. Here we provide a comprehensive assessment of responses of GPR55 knockout and wild-type mice to mechanical and thermal (heat, cold) stimulation in multiple, mechanistically distinct models of inflammatory and neuropathic pain. Inflammatory sensitization was produced by intraplantar administration of capsaicin, formalin or complete Freund’s adjuvant. No differences in responding were detected between GPR55 knockout and wild-type mice in any model of inflammatory nociception assessed. Neuropathic pain was induced by partial sciatic nerve ligation (which induces hypersensitivity to mechanical, cold and heat stimulation) or by treatment with the chemotherapeutic agent paclitaxel (which induces hypersensitivity to mechanical and cold stimulation only). No differences were observed between GPR55 knockout and wild type mice in either development or maintenance of neuropathic nociception in either neuropathic pain model. In conclusion, genetic deletion of GPR55 did not alter the development of pathological pain in adult mice in any chronic pain model evaluated.Lawrence M. CareyTannia GutierrezLiting DengWan-Hung LeeKen MackieAndrea G. HohmannNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lawrence M. Carey Tannia Gutierrez Liting Deng Wan-Hung Lee Ken Mackie Andrea G. Hohmann Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
description	Abstract The G-protein coupled receptor GPR55 has been postulated to serve as a novel cannabinoid receptor. A previous report indicated that GPR55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR55 in the control of nociceptive responding. However, GPR55 knockout mice remain incompletely characterized in models of pathological pain. Here we provide a comprehensive assessment of responses of GPR55 knockout and wild-type mice to mechanical and thermal (heat, cold) stimulation in multiple, mechanistically distinct models of inflammatory and neuropathic pain. Inflammatory sensitization was produced by intraplantar administration of capsaicin, formalin or complete Freund’s adjuvant. No differences in responding were detected between GPR55 knockout and wild-type mice in any model of inflammatory nociception assessed. Neuropathic pain was induced by partial sciatic nerve ligation (which induces hypersensitivity to mechanical, cold and heat stimulation) or by treatment with the chemotherapeutic agent paclitaxel (which induces hypersensitivity to mechanical and cold stimulation only). No differences were observed between GPR55 knockout and wild type mice in either development or maintenance of neuropathic nociception in either neuropathic pain model. In conclusion, genetic deletion of GPR55 did not alter the development of pathological pain in adult mice in any chronic pain model evaluated.
format	article
author	Lawrence M. Carey Tannia Gutierrez Liting Deng Wan-Hung Lee Ken Mackie Andrea G. Hohmann
author_facet	Lawrence M. Carey Tannia Gutierrez Liting Deng Wan-Hung Lee Ken Mackie Andrea G. Hohmann
author_sort	Lawrence M. Carey
title	Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
title_short	Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
title_full	Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
title_fullStr	Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
title_full_unstemmed	Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice
title_sort	inflammatory and neuropathic nociception is preserved in gpr55 knockout mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/4b5b7f6227954b9f86d12bdebdc63a59
work_keys_str_mv	AT lawrencemcarey inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice AT tanniagutierrez inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice AT litingdeng inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice AT wanhunglee inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice AT kenmackie inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice AT andreaghohmann inflammatoryandneuropathicnociceptionispreservedingpr55knockoutmice
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Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice

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