Abstract

There are many evidences which indicate that calcium channel related voltage plays an important role on the mechanism of neuropathic pain, but no strong evidence has been found yet on the role played by type-L calcium channel. The aim of this study was to evaluate this role in using a properly designed experiment. This cohort study was carried out on seven groups (eight  animals each) of male Wistar rats (200 to300 g). Chronic constriction nerve injury was performed on rats by loosely ligating their common sciatic nerve. The impact of corticosteron at 15 mg/kg on neuropathic pain behaviors was assessed in the presence or absence of verapamil as an L-VSC channel blocker at 5, 10 or 20 mg/kg. Standard procedures were employed to evaluate the behavioral pain responses including the thermal hyperalgesia and the thermal and mechanical allodynia. Our findings indicate that peripheral administration of corticosterone suppressed both hyperalgesia, and thermal and mechanical allodynia; however, verapamil pretreatment attenuated the effects of corticosterone on both thermal hyperalgesia and mechanical allodynia. In addition, the administration of verapamil alone at high dose (20 mg) suppressed both thermal and mechanical allodynia. These findings show that the inhibitory effects of glucocorticoids on neuropathic pain behaviors, at least in part, may be mediated through L-type VSC channels; but our findings suggest a potential role for glucocorticoids receptors agonists in combination with L-type VSC channels antagonists in the clinical management of neuropathic pain.

Key words: Corticosterone, L-type, calcium channel, mechanical allodynia, thermal allodynia, thermal hyperalgesia.