Involvement of microglia and interleukin-18 in the induction of long-term potentiation of spinal nociceptive responses induced by tetanic sciatic stimulation

Chu, Yu‐Xia; Zhang, Yu‐Qiu

doi:10.1007/s12264-012-1058-4

Cited by 25 publications

(17 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some published data showed that administration of IL-18 leads to increased microglial activation (Prinz and Hanisch, 1999). Studies suggest that IL-18 released by microglial cells is responsible for the development of allodynia (Miyoshi et al, 2008;Chu et al, 2012;Daigo et al 2012), which is consistent with our results. On day 7 following CCI, the IL-18 mRNA levels in the spinal cord and DRG increase and are reduced by minocycline administration.…”

Section: Discussionsupporting

confidence: 93%

Involvement of pro- and antinociceptive factors in minocycline analgesia in rat neuropathic pain model

Rojewska

Popiołek-Barczyk

Jurga

et al. 2014

Journal of Neuroimmunology

102

View full text Add to dashboard Cite

In neuropathic pain the repeated minocycline treatment inhibited the mRNA and protein expression of the microglial markers and metalloproteinase-9 (MMP-9). The minocycline diminished the pronociceptive (IL-6, IL-18), but not antinociceptive (IL-1alpha, IL-4, IL-10) cytokines at the spinal cord level. In vitro primary cell culture studies have shown that MMP-9, TIMP-1, IL-1beta, IL-1alpha, IL-6, IL-10, and IL-18 are of microglial origin. Minocycline reduces the production of pronociceptive factors, resulting in a more potent antinociceptive effect. This change in the ratio between pro- and antinociceptive factors, in favour of the latter may be the mechanism of minocycline analgesia in neuropathy.

show abstract

Section: Discussionsupporting

confidence: 93%

Involvement of pro- and antinociceptive factors in minocycline analgesia in rat neuropathic pain model

Rojewska

Popiołek-Barczyk

Jurga

et al. 2014

Journal of Neuroimmunology

102

View full text Add to dashboard Cite

show abstract

“…IL-18 is highly related to IL-1β, and both require caspase-1 and inflammasomes for active cleavage[146]. Nerve injury induces IL-18 expression in spinal microglia[34,167]. Furthermore, painful injuries induce cytokine expression in peripheral glia.…”

Section: Different Activation States Of Glia After Painful Stimulimentioning

confidence: 99%

Glia and pain: Is chronic pain a gliopathy?

Berta

2013

Pain

971

900

View full text Add to dashboard Cite

Activation of glial cells and neuro-glial interactions are emerging as key mechanisms underlying chronic pain. Accumulating evidence has implicated 3 types of glial cells in the development and maintenance of chronic pain: microglia and astrocytes of the central nervous system (CNS), and satellite glial cells of the dorsal root and trigeminal ganglia. Painful syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2) phosphorylation of mitogen-activated protein kinase signaling pathways; (3) upregulation of adenosine triphosphate and chemokine receptors and hemichannels and downregulation of glutamate transporters; and (4) synthesis and release of glial mediators (eg, cytokines, chemokines, growth factors, and proteases) to the extracellular space. Although widely detected in chronic pain resulting from nerve trauma, inflammation, cancer, and chemotherapy in rodents, and more recently, human immunodeficiency virus-associated neuropathy in human beings, glial reaction (activation state 1) is not thought to mediate pain sensitivity directly. Instead, activation states 2 to 4 have been demonstrated to enhance pain sensitivity via a number of synergistic neuro-glial interactions. Glial mediators have been shown to powerfully modulate excitatory and inhibitory synaptic transmission at presynaptic, postsynaptic, and extrasynaptic sites. Glial activation also occurs in acute pain conditions, and acute opioid treatment activates peripheral glia to mask opioid analgesia. Thus, chronic pain could be a result of “gliopathy,” that is, dysregulation of glial functions in the central and peripheral nervous system. In this review, we provide an update on recent advances and discuss remaining questions.

show abstract

“…It was subsequently reported that the inhibitory effect of IL-18 on LTP could be attenuated by the mGluR5 specific antagonist MPEP and the group II mGluR antagonist, MTPG (Cumiskey et al, 2007c) and also by the COX-2 inhibitor, SC-236, the iNOS inhibitor 1400W and peroxisome proliferation activated receptor (PPAR)γ agonist, ciglitazone (Cumiskey et al, 2007b). Interestingly IL-18 also inhibits LTP of C-fiber-evoked field potentials induced by tetanic stimulation of the sciatic nerve in the spinal cord and the authors identified a key role for microglial activation since IL-18 was localized largely to microglia and this effect was inhibited by minocycline (Chu et al, 2012).…”

Section: Il-1β Il-18 the Inflammasome And Ltpmentioning

confidence: 99%

Neuroinflammatory changes negatively impact on LTP: A focus on IL-1β

Lynch

2015

Brain Research

View full text Add to dashboard Cite

Involvement of microglia and interleukin-18 in the induction of long-term potentiation of spinal nociceptive responses induced by tetanic sciatic stimulation

Cited by 25 publications

References 51 publications

Involvement of pro- and antinociceptive factors in minocycline analgesia in rat neuropathic pain model

Involvement of pro- and antinociceptive factors in minocycline analgesia in rat neuropathic pain model

Glia and pain: Is chronic pain a gliopathy?

Neuroinflammatory changes negatively impact on LTP: A focus on IL-1β

Contact Info

Product

Resources

About