https://doi.org/10.5812/koomesh-154029

Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, I.R. Iran

authors:

avatar Monireh Naderitehrani 1 , avatar Azhdar Heydari 2 , avatar Saeedeh Nasrollahi 2 , avatar Zahra Esmaili 2 , avatar Gholamali Hamidi 1 , *

Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, I.R. Iran
Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, I.R. Iran Introduction : Damage to the central and peripheral nervous system causes neuropathic pain. Caffeine is a plant alkaloid and non -selective antagonist of A1, A2a and A2b adenosine receptors. It is reported that caffeine increase s the threshold of pain. In this study, the effect of acute caffeine on behavioral responses of neuropathic pain was investigated . Materials and Methods : The present study was conducted on 56 adult male Wistar rats in the weight range of 220 -250 g. Neuropathic pain was induced by chronic constriction injury (CCI (. Animals were randomly divided into 7 groups (n = 8): Control, Sham , CCI, CCI + Saline, and CCI + Caffeine (10, 50 and 100 mg/kg). Thermal hyperalgesia, mechanical and thermal allodynia has been done on days 4 ,7, 14, 21, 28 after CCI . Results: Neuropathic rats desmostrated increased pain thresholds. Notably, caffeine at a dose of 10 mg/kg significantly increased the thermal allodynia., but at doses of 50 and 100 mg/kg, it significantly decreased the thermal hyperalgesia and mechanical allodynia. Conclusion: Our findings indicated that the effects of caffeine on pain responses are dose -dependent. Probably the inhibition of adenosine A1 receptors by caffeine increase s pain responses, while the inhibition of A2a and A2b adenosine receptors is associated with protective effect of caffeine against pain responses. Keywords : Neuropathic pain, Hyperalgesia, Allodynia, Caffeine, Wistar Rats . * Corresponding author. +98 9131631685 hamiidi@yahoo.com Received:22 Apr 2019; Accepted
Koomesh: Vol.22, issue 2; e154029
published online: August 24, 2020
article type: Research Article

how to cite: Naderitehrani M, Heydari A, Nasrollahi S, Esmaili Z, Hamidi G. Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, I.R. Iran. koomesh. 2020;22(2):e154029. https://doi.org/10.5812/koomesh-154029.

Abstract

Introduction: Damage to the central and peripheral nervous system causes neuropathic pain. Caffeine is a plant alkaloid and non-selective antagonist of A1, A2a and A2b adenosine receptors. It is reported that caffeine increases the threshold of pain. In this study, the effect of acute caffeine on behavioral responses of neuropathic pain was investigated. Materials and Methods: The present study was conducted on 56 adult male Wistar rats in the weight range of 220-250 g. Neuropathic pain was induced by chronic constriction injury (CCI(. Animals were randomly divided into 7 groups (n = 8): Control, Sham, CCI, CCI + Saline, and CCI + Caffeine (10, 50 and 100 mg/kg). Thermal hyperalgesia, mechanical and thermal allodynia has been done on days 4 ,7, 14, 21, 28 after CCI. Results: Neuropathic rats desmostrated increased pain thresholds. Notably, caffeine at a dose of 10 mg/kg significantly increased the thermal allodynia., but at doses of 50 and 100 mg/kg, it significantly decreased the thermal hyperalgesia and mechanical allodynia. Conclusion: Our findings indicated that the effects of caffeine on pain responses are dose-dependent. Probably the inhibition of adenosine A1 receptors by caffeine increases pain responses, while the inhibition of A2a and A2b adenosine receptors is associated with protective effect of caffeine against pain responses.