Review Article
Targeting the Endocannabinoid System for Prevention or Treatment of Chemotherapy-Induced Neuropathic Pain: Studies in Animal Models
Table 1
Expression of endocannabinoids in animal models of CINP.
| CINP model | Expression of endocannabinoids | Reference | Chemotherapy drug | Animals | CINP symptom | Tissue | Change in endocannabinoid levels relative to control |
| Cisplatin | Male C3H/HeN mice | Mechanical and heat hyperalgesia | Plantar paw skin | Decrease in AEA but no change in 2-AG | [25] | Cisplatin | Male SD rats | Mechanical and cold allodynia | Lumbar spinal cord | Both 2-AG and AEA increased | [24] | Dorsal hind paw skin | 2-AG decreased but not AEA | Cisplatin | Male C3H/HeN mice | Mechanical hyperalgesia | Plantar paw skin | Both 2-AG and AEA decreased | [26] | DRGs | Both 2-AG and AEA decreased | Lumbar spinal cord | Both 2-AG and AEA increased | Midbrain | No effect on both 2-AG and AEA | Cisplatin | Male C3H/HeJ mice | Mechanical allodynia | Plantar paw skin | Decrease in AEA but no change in 2-AG | [27] |
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2-AG, 2-arachidonoylglycerol; AEA, N-arachidonoylethanolamine (anandamide); SD, Sprague-Dawley.
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