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, 2011, 468061

Activation of Mitogen-Activated Protein Kinase in Descending Pain Modulatory System

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Activation of Mitogen-Activated Protein Kinase in Descending Pain Modulatory System

Hiroki Imbe et al. J Signal Transduct.

Abstract

The descending pain modulatory system is thought to undergo plastic changes following peripheral tissue injury and exerts bidirectional (facilitatory and inhibitory) influence on spinal nociceptive transmission. The mitogen-activated protein kinases (MAPKs) superfamily consists of four main members: the extracellular signal-regulated protein kinase1/2 (ERK1/2), the c-Jun N-terminal kinases (JNKs), the p38 MAPKs, and the ERK5. MAPKs not only regulate cell proliferation and survival but also play important roles in synaptic plasticity and memory formation. Recently, many studies have demonstrated that noxious stimuli activate MAPKs in several brain regions that are components of descending pain modulatory system. They are involved in pain perception and pain-related emotional responses. In addition, psychophysical stress also activates MAPKs in these brain structures. Greater appreciation of the convergence of mechanisms between noxious stimuli- and psychological stress-induced neuroplasticity is likely to lead to the identification of novel targets for a variety of pain syndromes.

Figures

Figure 1
Figure 1
(a) Time courses of p-ERK1/2 and p-p38 MAPK in the RVM after CFA injection into the hindpaw. (b) Photomicrographs showing p-ERK1/2- and p-p38 MAPK-immunoreactive neurons in the RVM (bregma −11.00 mm) following hindpaw inflammation. Scale  bar = 100 μm.
Figure 2
Figure 2
Schematic drawing of noxious stimuli-induced MAPKs activations in the descending pain modulatory system. Boxes indicate noxious stimulation, activated MAPK, and function that is related to MAPK activation. PFC, prefrontal cortex; ACC, anterior cingulate cortex; AMY, amygdala; HPT, hypothalamus; PAG, periaqueductal gray; LC, locus coeruleus; RVM, rostral ventromedial medulla; DLF, dorsolateral funiculus; SDH, spinal dorsal horn; PAF, primary afferent fiber; POMC, proopiomelanocortin. Upward and downward arrowheads indicate increase and decrease, respectively.
Figure 3
Figure 3
Schematic drawing of stress-induced MAPKs activations in the descending pain modulatory system. Boxes indicate psychophysical stress, activated MAPK, and function that is related to MAPK activation. For abbreviations see Figure 2.

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References

    1. Fields HL, Basbaum AI. Central nervous system mechanisms of pain modulation. In: Wall PD, Melzack R, editors. Text Book of Pain. London, UK: Harcourt Publishers; 1999. pp. 309–329.
    1. Millan MJ. Descending control of pain. Progress in Neurobiology. 2002;66(6):355–474. - PubMed
    1. Ren K, Dubner R. Descending modulation in persistent pain: an update. Pain. 2002;100(1-2):1–6. - PubMed
    1. Porreca F, Ossipov MH, Gebhart GF. Chronic pain and medullary descending facilitation. Trends in Neurosciences. 2002;25(6):319–325. - PubMed
    1. Terayama R, Guan Y, Dubner R, Ren K. Activity-induced plasticity in brain stem pain modulatory circuitry after inflammation. NeuroReport. 2000;11(9):1915–1919. - PubMed
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