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首页> 外文期刊>Neuron >Muscarinic supersensitivity and impaired receptor desensitization in G protein-coupled receptor kinase 5-deficient mice.
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Muscarinic supersensitivity and impaired receptor desensitization in G protein-coupled receptor kinase 5-deficient mice.

机译：毒蕈碱超敏性和G蛋白偶联受体激酶5缺陷小鼠的受体脱敏受损。

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摘要

G protein-coupled receptor kinase 5 (GRK5) is a member of a family of enzymes that phosphorylate activated G protein-coupled receptors (GPCR). To address the physiological importance of GRK5-mediated regulation of GPCRs, mice bearing targeted deletion of the GRK5 gene (GRK5-KO) were generated. GRK5-KO mice exhibited mild spontaneous hypothermia as well as pronounced behavioral supersensitivity upon challenge with the nonselective muscarinic agonist oxotremorine. Classical cholinergic responses such as hypothermia, hypoactivity, tremor, and salivation were enhanced in GRK5-KO animals. The antinociceptive effect of oxotremorine was also potentiated and prolonged. Muscarinic receptors in brains from GRK5-KO mice resisted oxotremorine-induced desensitization, as assessed by oxotremorine-stimulated [5S]GTPgammaS binding. These data demonstrate that elimination of GRK5 results in cholinergic supersensitivity and impaired muscarinic receptor desensitization and suggest that a deficit of GPCR desensitization may be an underlying cause of behavioral supersensitivity.
机译：G蛋白偶联受体激酶5（GRK5）是磷酸化活化G蛋白偶联受体（GPCR）的酶家族的成员。为了解决GRK5介导的GPCR调控的生理重要性，生成了带有GRK5基因靶向缺失（GRK5-KO）的小鼠。当用非选择性毒蕈碱激动剂oxotremorine攻击时，GRK5-KO小鼠表现出轻度的自发性体温过低以及明显的行为超敏性。 GRK5-KO动物增强了经典的胆碱能反应，例如体温过低，活动不足，震颤和流涎。 oxotremorine的抗伤害感受作用也得到增强和延长。 GRK5-KO小鼠的大脑中的毒蕈碱受体可抵抗草嘌呤引起的脱敏反应，这是通过草嘌呤刺激的[5S] GTPgammaS结合来评估的。这些数据表明，消除GRK5会导致胆碱能超敏反应和毒蕈碱受体脱敏作用受损，并表明GPCR脱敏作用不足可能是行为超敏反应的根本原因。

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