Prophylactic cannabinoid administration blocks the development of paclitaxel-induced neuropathic nociception during analgesic treatment and following cessation of drug delivery

Antzeko izenburuak

• Selective Activation of Cannabinoid CB(2) Receptors Suppresses Neuropathic Nociception Induced by Treatment with the Chemotherapeutic Agent Paclitaxel in Rats
  nork: Rahn, Elizabeth J., et al.
  Argitaratua: (2008)
• Prophylactic treatment with the tricyclic antidepressant desipramine prevents development of paclitaxel-induced neuropathic pain through activation of endogenous analgesic systems
  nork: Deng, Liting, et al.
  Argitaratua: (2016)
• The maintenance of cisplatin- and paclitaxel-induced mechanical and cold allodynia is suppressed by cannabinoid CB(2) receptor activation and independent of CXCR4 signaling in models of chemotherapy-induced peripheral neuropathy
  nork: Deng, Liting, et al.
  Argitaratua: (2012)
• Activation of cannabinoid CB(1) and CB(2) receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats
  nork: Rahn, E J, et al.
  Argitaratua: (2007)
• Brain-Permeant and -Impermeant Inhibitors of Fatty Acid Amide Hydrolase Synergize with the Opioid Analgesic Morphine to Suppress Chemotherapy-Induced Neuropathic Nociception Without Enhancing Effects of Morphine on Gastrointestinal Transit
  nork: Slivicki, Richard A., et al.
  Argitaratua: (2018)