BACKGROUND:Studies have reported that potassium channel openers exhibit a protective effect on cerebral ischemia-reperfusion injury and inhibit glutamate excitotoxicity in rats.However,the effects of the glutamate receptor 1α and glutamate transporter 1 remain poorly understood.OBJECTIVE:To investigate the prophylactic use of the adenosine triphosphate-sensitive potassium channel opener cromakalim on neurological function and cerebral infarct size,as well as glutamate receptor 1α and glutamate transporter 1 expression,in rats with cerebral ischemia-reperfusion injury,and to explore action mechanisms underlying reduced glutamate excitotoxicity and neuroprotection in rats.DESIGN,TIME AND SETTING:Randomized,controlled,animal experiment was performed at the Brain Institute,Qingdao University Medical College,Between July 2008 and April 2009.MATERIALS:Cromakalim was purchased from Sigma,USA;rabbit anti-glutamate receptor 1α polyclonal antibody was offered by Wuhan Boster,China;rabbit anti-glutamate transporter 1 polyclonal antibody was offered by Santa Cruz Biotechnology,USA.METHODS:Sixty male,Wistar rats,aged 6 months,were randomly assigned to three groups (n= 20):sham-surgery,model,and cromakalim.Intraluminal thread methods were used to establish middle cerebral artery occlusion in rats from the model and cromakalim groups.Rats from the sham-surgery group were subjected to exposed common carotid artery,external carotid artery,and internal carotid artery,without occlusion.Cromakalim (10 mg/kg) was administered 30 minutes prior to middle cerebral artery occlusion,but there was no intervention in the model and sham-surgery groups.MAIN OUTCOME MEASURES:At 24 hours post-surgery,neurological behavioral functions were evaluated using Bederson’s test,cerebral infarction volume was determined following tetrazolium chloride staining,and glutamate receptor 1α and glutamate transporter 1 expressions were detected using immunohistochemistry.RESULTS:Following cerebral ischemia-reperfusion injury,neurological behavioral malfunctions were obvious in all mice.Focal cerebral infarction was detected in ischemic hemispheres,glutamate receptor 1α expression increased,and glutamate transporter 1 expression decreased in the ischemic hemisphere (P < 0.05).Compared with the model group,neurological behavioral functions significantly improved,cerebral infarction volume was significantly reduced (P < 0.05),glutamate receptor 1α expression was significantly decreased,and glutamate transporter 1 expression was increased in the cromakalim group (P < 0.05).CONCLUSION:Improved neurological function and reduced cerebral infarction volume in rats through the preventive use of cromakalim could be related to decreased glutamate receptor 1α expression and enhanced glutamate transporter 1 expression. BACKGROUND: Studies have reported that potassium channel openers exhibit a protective effect on cerebral ischemia-reperfusion injury and inhibit glutamate excitotoxicity in rats. However, the effects of the glutamate receptor 1α and glutamate transporter 1 remain poorly understood. OBJECTIVE: To investigate the prophylactic use of the adenosine triphosphate-sensitive potassium channel opener cromakalim on neurological function and cerebral infarct size, as well as glutamate receptor 1α and glutamate transporter 1 expression, in rats with cerebral ischemia-reperfusion injury, and to explore the action mechanisms underlying reduced glutamate excitotoxicity and neuroprotection in rats. DESI, TIME AND SETTING: Randomized, controlled, animal experiment was performed at the Brain Institute, Qingdao University Medical College, Between July 2008 and April 2009. MAIALIALS: Cromakalim was purchased from Sigma, USA; rabbit anti-glutamate receptor 1α polyclonal antibody was offered by Wuhan Boster, China; rabbit anti -glutamate transporter 1 polyclonal antibody was offered by Santa Cruz Biotechnology, USA. METHODS: Sixty male, Wistar rats, aged 6 months, were randomly assigned to three groups (n = 20): sham-surgery, model, and cromakalim. Intraluminal thread methods were used to establish middle cerebral artery occlusion in rats from the model and cromakalim groups. Rats from the sham-surgery group were subjected to exposed common carotid artery, external carotid artery, and internal carotid artery, without occlusion. Cromakalim (10 mg / kg) was administered 30 minutes prior to middle cerebral artery occlusion, but there was no intervention in the model and sham-surgery groups. MAIN OUTCOME MEASURES: At 24 hours post-surgery, neurological behavioral functions were evaluated using Bederson’s test, cerebral infarction volume was determined following tetrazolium chloride staining, and glutamate receptor 1α and glutamate transporter 1 expressions were detected using immunohistochemistry. RESULTS: Following cerebral ischemia-re perfusion injury, neurological behavioral malfunctions were significantly in all mice. Focal cerebral infarction was detected in ischemic hemispheres, glutamate receptor 1α expression increased, and glutamate transporter 1 decreased in the ischemic hemisphere (P <0.05) .Compared with the model group, neurological (P <0.05). CONCLUSION: Improved neurological function and reduced cerebral (P <0.05), glutamate receptor 1α expression was significantly decreased, and glutamate transporter 1 expression was increased in the cromakalim group infarction volume in rats through the preventive use of cromakalim could be related to decreased glutamate receptor 1α expression and enhanced glutamate transporter 1 expression.