The present study was designed to investigate the possible role of
opioids and K(
ATP) channels in
ischemic postconditioning-induced reversal of global
cerebral ischemia and reperfusion (I/R) induced neuronal injury. Mice were subjected to global
ischemia by bilateral carotid artery occlusion for 10 min followed by reperfusion for 24 h, to produce neuronal injury.
Ischemic postconditioning was induced by three episodes of carotid artery occlusion and reperfusion of 10 s each, immediately after global
ischemia.
Morphine postconditioning was induced by administration of
morphine (5 mg/kg i.v.), 5 min prior to reperfusion.
Naloxone (5 mg/kg i.v.),
opioid receptor antagonist, and
glibenclamide (5 mg/kg i.v.), K(
ATP) channel blocker were administered 10 min before global
ischemia. Extent of cerebral injury was assessed by measuring
cerebral infarct size using triphenyl tetrazolium
chloride (TTC) staining. Short-term memory was evaluated using the elevated plus maze test, while degree of motor
incoordination was evaluated using inclined beam-walking, rota-rod and lateral push tests. Bilateral carotid artery occlusion followed by reperfusion resulted in significant increase in
infarct size, impairment in short-term memory and motor co-ordination. Ischemic/
morphine postconditioning significantly attenuated I/R induced neuronal injury and behavioural alterations. Pretreatments with
naloxone and
glibenclamide attenuated the
neuroprotective effects of ischemic/
morphine postconditioning. It may be concluded that ischemic/
morphine postconditioning protects I/R induced cerebral injury via activating
opioid receptor and K(
ATP) channel opening.