Chemotherapy-induced pain is promoted by enhanced spinal adenosine kinase levels via astrocyte-dependent mechanisms

Míreanna Comhchosúla

• A(3) adenosine receptor agonist prevents the development of paclitaxel-induced neuropathic pain by modulating spinal glial-restricted redox-dependent signaling pathways
  le: Janes, Kali, et al.
  Foilsithe: (2014)
• Spinal neuroimmmune activation is independent of T-cell infiltration and attenuated by A3 adenosine receptor agonists in a model of oxaliplatin-induced peripheral neuropathy
  le: Janes, Kali, et al.
  Foilsithe: (2014)
• Controlling murine and rat chronic pain through A(3) adenosine receptor activation
  le: Chen, Zhoumou, et al.
  Foilsithe: (2012)
• Spinal NADPH Oxidase is a Source of Superoxide in the Development of Morphine-Induced Hyperalgesia and Antinociceptive Tolerance
  le: Doyle, Tim, et al.
  Foilsithe: (2010)
• Bioenergetic deficits in peripheral nerve sensory axons during chemotherapy-induced neuropathic pain resulting from peroxynitrite-mediated post-translational nitration of mitochondrial superoxide dismutase
  le: Janes, Kali, et al.
  Foilsithe: (2013)