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Cytokine and chemokine regulation of sensory neuron function

 Richard J. Miller  ;  Hosung Jung  ;  Sonia K. Bhangoo  ;  Fletcher A. White 
 Handbook of Experimental Pharmacology, Vol.194 : 417-449, 2009 
Journal Title
Handbook of Experimental Pharmacology
Issue Date
Acute Disease ; Analgesics/pharmacology ; Animals ; Anti-Inflammatory Agents/pharmacology ; Chemokines/metabolism* ; Chronic Disease ; Cytokines/metabolism* ; Ganglia, Spinal/immunology ; Humans ; Hyperalgesia/immunology ; Hyperalgesia/prevention & control ; Inflammation/immunology ; Inflammation/prevention & control ; Inflammation Mediators/metabolism* ; Neuralgia/immunology* ; Neuralgia/physiopathology ; Neuralgia/prevention & control ; Neuroglia/immunology ; Pain Threshold ; Receptors, Chemokine/metabolism ; Receptors, Cytokine/metabolism ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/immunology* ; Signal Transduction*/drug effects ; Syndrome
Cytokine ; Chemokine ; DRG ; Pain ; Inflammation
Pain normally subserves a vital role in the survival of the organism, prompting the avoidance of situations associated with tissue damage. However, the sensation of pain can become dissociated from its normal physiological role. In conditions of neuropathic pain, spontaneous or hypersensitive pain behavior occurs in the absence of the appropriate stimuli. Our incomplete understanding of the mechanisms underlying chronic pain hypersensitivity accounts for the general ineffectiveness of currently available options for the treatment of chronic pain syndromes. Despite its complex pathophysiological nature, it is clear that neuropathic pain is associated with short- and long-term changes in the excitability of sensory neurons in the dorsal root ganglia (DRG) as well as their central connections. Recent evidence suggests that the upregulated expression of inflammatory cytokines in association with tissue damage or infection triggers the observed hyperexcitability of pain sensory neurons. The actions of inflammatory cytokines synthesized by DRG neurons and associated glial cells, as well as by astrocytes and microglia in the spinal cord, can produce changes in the excitability of nociceptive sensory neurons. These changes include rapid alterations in the properties of ion channels expressed by these neurons, as well as longer-term changes resulting from new gene transcription. In this chapter we review the diverse changes produced by inflammatory cytokines in the behavior of sensory neurons in the context of chronic pain syndromes
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1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
Yonsei Authors
Jung, Ho Sung(정호성) ORCID logo https://orcid.org/0000-0002-5059-8050
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