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چکیده:  
Background: Partial peripheral nerve injury often results in chronic pain, including hyperalgesia and allodynia. Caffeine as a non-selective antagonist of adenosine receptors (ARs) has protective effects on neuropathic pain. Since, in the central effects of caffeine nitric oxide (NO) partially is involved, we therefore investigated the effects of acute caffeine administration on neuropathic pain, focusing on A1 and A2 receptors and the possible role of NO.
Methods: Following chronic constriction injury (CCI), male Wistar rats were administrated with caffeine (10, 50 and 100mg/kg). Also, groups of animals received L-NAME (30mg/kg) or L-arginine (100mg/kg) either alone or as before treatment with 50 mg/kg of caffeine. Rats were tested for hyperalgesia and allodynia at 4, 7, 14, 21 and 28 days following CCI.
Results: Administration of 10 mg/kg of caffeine significantly increased cold allodynia, while 50 and 100 mg/kg of caffeine, decreased mechanical allodynia and thermal hyperalgesia. Pre-treatment with L-NAME before caffeine administration decreased cold and mechanical allodynia, and thermal hyperalgesia. Treatment with L-arginine before caffeine administration, increased thermal hyperalgesia and decreased cold allodynia.
Conclusions: The present data show that caffeine dose-dependently affects the pro-analgesic or anti-analgesic states in the CCI model.
نوع مطالعه: Original | موضوع مقاله: Behavioral Neuroscience
دریافت: 1402/2/12 | پذیرش: 1402/3/9

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