神经病理性疼痛
背根神经节
甘丙肽
医学
伤害
孤儿受体
神经损伤
受体
脊髓
内分泌学
内科学
神经肽
麻醉
神经科学
生物
精神科
基因
转录因子
生物化学
作者
Fiona E. Holmes,Niall C. H. Kerr,Ying‐Ju Chen,Penny A. Vanderplank,Craig Alexander McArdle,David Wynick
标识
DOI:10.1016/j.mcn.2016.11.010
摘要
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 7days 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 100nM and 10μM 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.
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