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Published on: July 31, 2017
Possible role of opioids and KATP channels in neuroprotective effect of postconditioning in mice
Bharat Bhai Pateliya1, Nirmal Singh, Amteshwar Singh Jaggi
1Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Abstract:
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.
Insights
Ischemic postconditioning, using opioids like morphine, protects the brain from injury caused by interrupted blood flow (ischemia and reperfusion). This protection involves opioid receptors and K(ATP) channels.
Area of Science:
- Neuroscience
- Pharmacology
- Cardiovascular Research
Background:
- Global cerebral ischemia and reperfusion (I/R) cause significant neuronal injury.
- Postconditioning strategies are explored to mitigate I/R-induced damage.
- The roles of opioids and K(ATP) channels in neuroprotection are not fully understood.
Purpose of the Study:
- To investigate the neuroprotective mechanisms of ischemic and morphine postconditioning against global cerebral I/R injury.
- To determine the involvement of opioid receptors and K(ATP) channels in these protective effects.
Main Methods:
- Global cerebral ischemia was induced in mice via bilateral carotid artery occlusion, followed by reperfusion.
- Ischemic postconditioning involved brief, repeated occlusions/reperfusions; morphine postconditioning used intravenous morphine.
- Neuroprotection was assessed by infarct size (TTC staining) and behavioral tests (memory, motor coordination).
- Opioid receptor antagonist (naloxone) and K(ATP) channel blocker (glibenclamide) were used to probe mechanisms.
Main Results:
- I/R significantly increased infarct size and impaired memory and motor coordination.
- Ischemic and morphine postconditioning markedly reduced I/R-induced neuronal injury and behavioral deficits.
- Pretreatment with naloxone or glibenclamide diminished the neuroprotective effects of postconditioning.
Conclusions:
- Ischemic and morphine postconditioning offer significant neuroprotection against global cerebral I/R injury.
- Opioid receptors and K(ATP) channels are critical mediators of this neuroprotection.
- Targeting these pathways may represent a therapeutic strategy for stroke and related conditions.
