Spinal Glial Activation Contributes to Postoperative Mechanical Hypersensitivity in the Rat

Obata, Hideaki; Eisenach, James C.; Hussain, Hesham; Bynum, Tanishua; Vincler, Michelle

doi:10.1016/j.jpain.2006.04.004

Cited by 120 publications

(93 citation statements)

References 32 publications

(30 reference statements)

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“…By that, a proliferative growth and hypertrophia of glial cells is induced in the CNS which in turn release more pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 and thereby also contribute to the complex activation loop. [21][22][23] TNF-α, IL-6, and IL-1β are potent COX-2 activators 24 (see Fig. 1B) and consequently also prostaglandins accumulate in both injured tissue and spinal cord leading to an increased sensibility of neurons.…”

Section: Pain and Inflammationmentioning

confidence: 99%

IL-4, JAK-STAT signaling, and pain

Busch-Dienstfertig

González-Rodríguez

2013

JAK-STAT

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Section: Pain and Inflammationmentioning

confidence: 99%

IL-4, JAK-STAT signaling, and pain

Busch-Dienstfertig

González-Rodríguez

2013

JAK-STAT

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“…Nerve injuryinduced upregulation of OX-42 and Iba1 appears to be age-dependent: young rats show weak responses, which may explain why neuropathic pain is less robust in these animals Vega-Avelaira et al, 2006). Although OX-42 is the most used marker for microglia activation in different pain conditions, pain states can be dissociated from OX-42 changes in several cases (Colburn et al, 1997;Obata et al, 2006;Winkelstein & DeLeo, 2002). Indeed, OX-42 increase is more associated with nerve injury than correlated with the pain symptoms.…”

Section: Microglia Activation and Proliferation In The Spinal Cord Inmentioning

confidence: 99%

“…Fluorocitrate has been shown to alleviate pain behavior in animal models of inflammatory pain, neuropathic pain, and postoperative pain (Clark et al, 2007a;Meller et al, 1994;Milligan et al, 2003;Obata et al, 2006;Watkins et al, 1997). However, it fails to inhibit muscle pain, a pain condition that does not show any glial activation (Ledeboer et al, 2006).…”

Section: The Role Of Microglia In Pain Controlmentioning

confidence: 99%

Do glial cells control pain?

Wen²,

et al. 2007

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Management of chronic pain is a real challenge, and current treatments focusing on blocking neurotransmission in the pain pathway have only resulted in limited success. Activation of glia cells has been widely implicated in neuroinflammation in the central nervous system, leading to neruodegeneration in many disease conditions such as Alzheimer's and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β can not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as BDNF and bFGF that are produced by glia to protect neurons. Thus, glia cells can powerfully control pain when they are activated to produce various pain mediators. We will review accumulating evidence supporting an important role of microglia cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We will also discuss possible signaling mechanisms in particular MAP kinase pathways that are critical for glia control of pain. Investigating signaling mechanisms in microglia may lead to more effective management of devastating chronic pain.

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“…These changes in excitability occur in both young and old alike. Both peripheral (primary sensory neuron) and central (secondary order neuron) changes are present, and a broad spectrum of sensory fibers are affected (Treede et al 1992;Dougherty 2003;Nagakura et al 2008;Ririe et al 2008;Duarte et al 2005;Obata et al 2006;. Primary sensory neurons encode peripheral damage, but they also may play a role in maintaining an abnormal responsiveness state to protect the injured area and prevent further damage.…”

mentioning

confidence: 99%

Skin incision-induced receptive field responses of mechanosensitive peripheral neurons are developmentally regulated in the rat

Boada

Gutiérrez

Giffear

et al. 2012

Journal of Neurophysiology

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Boada MD, Gutierrez S, Giffear K, Eisenach JC, Ririe DG. Skin incision-induced receptive field responses of mechanosensitive peripheral neurons are developmentally regulated in the rat. J Neurophysiol 108: 1122-1129, 2012. First published June 6, 2012 doi:10.1152/jn.00399.2012.-Maturation of the nervous system results in changes in both central and peripheral processing. To better understand responses to injury in the young, developmental differences in the acute response to incision were investigated in both tactile and nociceptive myelinated peripheral mechanosensitive afferent neurons in vivo. Neuronal intrasomal recordings were performed in juvenile and infant rats in 34 L5 dorsal root ganglia, and each neuron was phenotypically defined. Neurons had a mechanosensitive receptive field in the glabrous skin on the plantar surface of the hind paw, which was characterized at baseline and for up to 45 min after incision. Fundamental maturational differences in the effect of incision were clear: in high-threshold nociceptive mechanoreceptors, the mechanical threshold decreased immediately and the receptive field size increased rapidly in juvenile rats but not in infant rats. Additionally, a divergence in changes in the instantaneous response frequency of tactile afferents occurred between the two ages. These differences may help explain maturational differences in responses to peripheral injury and suggest that differences in central nervous system responses may be partially mitigated by spatially confined and frequencydependent differences resulting from tactile and nociceptive mechanosensitive input. development; dorsal root ganglia; intracellular electrophysiology; maturation; peripheral nerve SKIN INJURY produces considerable changes in afferent signaling and processing that leads to a hyperexcitability state (Treede et al. 1992;Brennan et al. 2005). These changes in excitability occur in both young and old alike. Both peripheral (primary sensory neuron) and central (secondary order neuron) changes are present, and a broad spectrum of sensory fibers are affected (Treede et al.

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Spinal Glial Activation Contributes to Postoperative Mechanical Hypersensitivity in the Rat

Cited by 120 publications

References 32 publications

IL-4, JAK-STAT signaling, and pain

IL-4, JAK-STAT signaling, and pain

Do glial cells control pain?

Skin incision-induced receptive field responses of mechanosensitive peripheral neurons are developmentally regulated in the rat

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