Objective: 

The aim of this study was obtain evidence for explaining the neurochemical mechanism between sleep and pain by investigating the effects of WIN55-212,2, a cannabinoid substance, on 96-hours rapid eye movement (REM) sleep deprivation induced hyperalgesia.

Methods: 

Forty Wistar albino rats (weight range, 200-220 g) were used. Four experimental groups, each having 10 animals, were as folows: CONT, REM deprivation+Placebo; WIN1, REM deprivation+Win55 (1 mg/kg); WIN3, REM deprivation+Win55 (3 mg/kg); WIN10, REM deprivation+Win55 (10 mg/kg). All animals underwent pain threshold measurements by hot-plate test and REM sleep deprivation by modified multiple platform technique. Then, Group 1 had DMSO 50%, Group 2, 3 and 4 had 1 mg/kg, 3 mg/kg, and 10 mg/kg WIN55-212,2 intraperitoneal injection (5 mL/kg), respectively. Sixty minutes after drug administration, pain threshold measurements were repeated. Pain threshold measurements were tested by Kolmogorov-Smirnov, the difference between the mean results of study groups were tested by ANOVA. In addition, post-hoc Tukey test was used. P<0.05 accepted as statistically significant.

Results: 

Pain threshold values significantly decreased after REM-deprivation in CONT, WIN1 and WIN3 groups (9.4±1.5 vs 7.6±1.6; 12.0±3.3 vs 6.5±1.6; and 12.0±2.6 vs 6.7±1.1; p<0.05 for all), whereas in WIN10, hyperalgesia disappeared by 10 mg/kg i.p. Win-55 (11.3±3.0 vs 10.5±4.8; p>0.05).

Conclusions: 

Intraperitoneal 10 mg/kg WIN55-212,2 prevented REM sleep deprivation induced hyperalgesia which suggests a role for cannabinoids in pain modulation during REM sleep loss.