Spinal microglia activation-importance for chronic pain

• Autorzy: Mika J.
• Języki publikacji: EN

Abstrakty

EN

Pain may now be considered a neuro-immune disorder, since it is known that the activation of immune and immune-like glial cells in the dorsal root ganglia and spinal cord results in the release of both pro- and anti-inflammatory cytokines, as well as algesic and analgesic mediators. Our studies underline an important role of cytokines (IL-1alfa, IL-1beta, IL-4, IL-6, IL-10, IL-18, fractalkine and CCL2); complement components (C1q); metaloproteinases (MMP-2, -9) and many other factors, which become activated under neuropathic pain. Another novel approach for controlling neuropathic pain can be pharmacological attenuation of glial and immune cell activation. It has been found that propentofylline, pentoxifylline, fluorocitrate and minocycline suppress the development of neuropathic pain. The other way of pain control can be inhibition of transcription factor synthesis (NF-kappaB); kinase synthesis (p38MAPK) and protease activation (MMP9). Additionally, since it is known that the opioid-induced glial activation opposes opioid analgesia, some glial inhibitors, which are safe and clinically well tolerated, are proposed as potential useful ko-analgesic agents for opioid treatment of neuropathic pain. Our results support the idea that targeting microglial activation represents a novel and clinically promising method for enhancing analgesic effects of opioids in neuropathic pain. Acknowledgments: Supported by grant 2011/03/B/NZ4/00042 and statutory funds.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2013
• Tom: 73
• Numer: Suppl.1
• Opis fizyczny: p.11-12

Twórcy

autor

Mika J.

• Department of Pain Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland