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date: 26 February 2020

Abstract and Keywords

Scientists and clinicians have long used the level of hormones or the level of inflammatory mediators as an important parameter of functional activity of the neuro-endocrine or immune system. However, not much focus has been given to the role of the sensitivity of the target tissue, such as receptors or components of the intracellular signalosome. This is important because, as recent literature has shown, the sensitivity of the target tissue may change during pathological processes such as inflammation or chronic stress. This chapter focuses on changes in sensitivity of target tissue by focussing on a kinase known as G protein receptor kinase 2 (GRK2), which appears to be an important regulator of the severity and duration of inflammatory pain. GRK2 regulates the sensitivity of target systems, including immune and nervous systems, for signals given by G protein-coupled receptors via regulating receptor desensitization. In addition, GRK2 regulates intracellular signaling via direct effects on elements of the signalosome of the cell. The contribution of GRK2 to chronic pain is discussed in the context of the idea that regulation of the sensitivity of target systems is an important process during neuro-inflammation and should be taken into account when investigating neuro-immune communication in inflammatory pathologies.

Keywords: hyperalgesia, cellular signaling, neuro-inflammation, cellular signaling, Cre-Lox technology, G protein-coupled receptors, central sensitization, chronic pain

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