Gq rather than G11 preferentially mediates nociceptor sensitization
Background: The Gq/11-protein signaling mechanism is essential throughout the nervous system, but little is known about the contribution of the individual G-protein GPCR signaling branches towards nociceptor activation and their specific role on nociceptor sensitization. We aimed to unravel the cont...
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| Main Authors: | , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
25 October 2013
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| In: |
Molecular pain
Year: 2013, Volume: 9, Pages: 1-6 |
| ISSN: | 1744-8069 |
| DOI: | 10.1186/1744-8069-9-54 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1186/1744-8069-9-54
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| Author Notes: | Laura Nikita Wirotanseng, Rohini Kuner and Anke Tappe-Theodor |
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| 520 | |a Background: The Gq/11-protein signaling mechanism is essential throughout the nervous system, but little is known about the contribution of the individual G-protein GPCR signaling branches towards nociceptor activation and their specific role on nociceptor sensitization. We aimed to unravel the contribution of the Gq/11-signaling pathway towards nociceptor activation via a variety of classical inflammatory mediators signalling via different G-protein GPCRs and investigated the specific contribution of the individual Gq and G11, G-Proteins in nociceptors. Findings: Using different transgenic mouse lines, lacking Gαq, Gα11, or both α-subunit of the G-proteins in primary nociceptive neurons, we analyzed the mechanical- and heat-sensitivity upon application of different GPCR-agonists that are known to play an important role under inflammatory conditions (e.g. ATP, Glutamate, Serotonin etc.). We found that the Gq/11-GPCR signaling branch constitutes a primary role in the manifestation of mechanical allodynia and a minor role in the development of thermal hyperalgesia. Moreover, with respect to the mediators used here, the Gq-protein is the principle G-protein among the Gq/11-protein family in nociceptive neurons leading to nociceptor sensitization. Conclusions: Our results demonstrate that the Gq/11 signaling branch plays a primary role in nociceptor sensitization upon stimulation with classical GPCR ligands, contributing primarily towards the development of mechanically allodynia. Moreover, the deletion of the individual G-proteins led to the finding that the Gq-protein dominates the signalling machinery of the Gq/11 family of G-proteins in nociceptive neurons. | ||
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