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Measuring chemotherapy‐induced neuropathic pain and attenuation by cannabidiol using pain‐stimulated and paindepressed models in female C57Bl/6 mice
Author(s) -
Pavlenko Khristina,
Neelakantan Harshini,
Walker Ellen A.,
Ward Sara Jane
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.662.15
Subject(s) - neuropathic pain , allodynia , medicine , cannabidiol , peripheral neuropathy , antagonist , anesthesia , pharmacology , gabapentin , self administration , hyperalgesia , chemotherapy , nociception , receptor , endocrinology , cannabis , psychiatry , alternative medicine , pathology , diabetes mellitus
Paclitaxel (PAC) is associated with a chemotherapy‐induced peripheral neuropathy that can lead to the cessation of treatment in cancer patients, even in the absence of alternate therapies. Rodent models of PAC‐induced neuropathic pain have focused on stimulus‐evoked sensitivity measurements following systemic dosing of PAC, while the effect of chemotherapy‐induced neuropathy on pain‐depressed behaviors has not been characterized. Also, the phytocannabinoid cannabidiol (CBD) can reverse other types of neuropathic pain, but its effect on PAC‐induced neuropathy has not previously been investigated. We investigated the effect of CBD on PAC‐induced mechanical allodynia and PAC‐induced suppression of palatable food consumption. PAC administration (4.0 – 8.0 mg/kg × 4 injections, IP) led to the onset of mechanical allodynia as well as a suppression of palatable food consumption. Treatment with CBD (5.0 mg/kg IP) prevented the development of PAC‐induced mechanical allodynia and reversed PAC‐induced suppression of food consumption. The ability of CBD treatment to block PAC effects was attenuated by pretreatment with the 5‐HT1A antagonist WAY100635 (1.0 mg/kg IP), but not the CB1 antagonist SR141716 (3.0 mg/kg IP). In conclusion, CBD blocks PAC‐induced neuropathic pain using pain‐stimulated and pain‐depressed models, and these effects may be mediated by stimulation of 5‐ HT1A receptors.