جستجوی مقالات مرتبط با کلیدواژه "هیپرآلژزیای حرارتی" در نشریات گروه "پزشکی"

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. 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. 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. 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.

Previous studies have shown that glucocorticoids play an important role in neuropathic pain behaviors, but the underlying mechanisms are not known. The aim of this study was to determine the role of NMDA receptors in the effects of glucocorticoids on neuropathic pain behaviors in CCI model in rats. Male adult Wistar rats (200-300 gram) were used in this srudy. Chronic constriction nerve injury (CCI) rats were produced by loosely ligating a common sciatic nerve. Two weeks after inducing CCI, the effects of corticosterone in the presence or absence of MK-801 (a bloker of NMDA receptor) were studied. Behavioral pain responses (thermal hyperalgesia and thermal and mechanical allodynia) were studied using standard procedures. Findings indicated that peripheral administration of corticosterone suppressed both hyperalgeisa and allodynia in a dose-dependent manner. MK-801 (0.3 mg/kg) pretreatment attenuated the effects of corticosterone (15mg/kg) on both thermal hyperalgesia and mechanical allodynia. Also MK-801 alone suppressed thermal allodynia, but not thermal hyperalgesia and mechanical allodynia. These findings show that glucocorticoids play an important role in neuropathic pain behaviors. It seems that at least part of glucocorticoids effects on these behaviors may mediate through NMDA receptors suggesting an involvement of non-genomic mechanisms. Our findings suggest a potential role for glucocorticoid receptors agonist in combination of NMDA receptors antagonists in clinical management of neuropathic pain.