Abstract
Introduction: The mechanisms underlying the inhibitory effects of glucocorticoids on neuropathic pain are not clear. The aim of this study was to determine the role of L-type voltage sensitive calcium channels (VSC) in the effects of corticosterone on neuropathic pain behaviors in CCI model in rats. Materials and Methods: Male adult Wistar rats (200-300 gram) were used in this study. Chronic constriction nerve injury (CCI) was produced in the animals by loosely ligating in their common sciatic nerve. Two weeks after inducing CCI, the effects of corticosterone (15 mg/kg) on neuropathic pain behaviors were examined in the presence or absence of verapmil a blocker of L-VSC channels, at the dose of 5, 10, or 20 mg/kg. Behavioral pain responses including thermal hyperalgesia and thermal and mechanical allodynia, were studied using standard procedures. Results: Our findings indicated that peripheral administration of corticosterone suppresses both hyperalgeisa and allodynia. Verapmil pretreatment attenuated the effects of corticosterone on both thermal hyperalgesia and mechanical allodynia. In addition, the administration of verapmil alone and at high dose suppressed both thermal allodynia, and mechanical allodynia. Conclusion: These findings showed that inhibitory effects of glucocorticoids on neuropathic pain behaviors, at least in part, might mediate through L-type VSC channels. Our findings suggest a potential role for glucocorticoid receptors agonist in combination of L-type VSC channels antagonists in the clinical management of neuropathic pain.
Keywords
Corticosterone, L-type, Calcium channel, Mechanical allodynia, Thermal allodynia, Thermal hyperalgesia کورتیکوسترون، درد نوروپاتی، کانالهای کلسیمی، آلودینیای مکانیکی، هیپرآلژزیای حرارتی
Copyright
© 2008, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.