Effects Of XFM And XFM-Specific Narcotic Antagonists On NMDAR1&BDZR In Rats’ Different Brain Regions

The miniature pigs were relatively ideal experimental animals for building diseases models,to make them better applied in scientific research and clinical practice, the excelent anesthesia andanaleptic effect were required. XFM and XFM-specific antagonist agent had been developed, thestudy of their mechanism had gained a wide range of outcomes. The purpose of this study is toinvestigate the effect of XFM-anesthesia and XFM-specific antagonistic anti-anesthesia onN-methyl-D-aspartate receptor type I (NMDAR1) and benzodiazepines receptor (BDZR) in rats’different brain regions, thus to explore the the mechanism of XFM-anesthesia and XFM-specificantagonist anti-anesthesia.Wistar rats were used as experimental animals, XFM and XFM-specific antagonist were givenby intraperitoneal injection, immunohistochemical method was used to locate and initial-quantifyNMDAR1and BDZR expression, thus to explore the the mechanism of XFM-anesthesia andXFM-specific antagonist anti-anesthesia, experimental results were as follows.1. After intraperitoneal injection with XFM for anesthesia, compared with control group,significant decline of NMDAR1positive expression was observed in cerebral cortex, hippocampus,thalamus, cerebellum, while NMDAR1positive expression did not change significantly in thebrainstem. The positive expression levels of NMDAR1in cerebral cortex, cerebellum andthalamus increased significantly along with time after anesthesia while the positive expression ofNMDAR1decreased significantly in the hippocampal brain region.2. After intraperitoneal injection with XFM for anesthesia, significant increase of BDZRpositive expression was showed firstly in cerebral cortex, hippocampus, thalamus compared withcontrol group. The positive expression levels of BDZR in cortex, hippocampus, thalamusdecreased siginificantly after significantly ascending. The positive expression of BDZR showed nosignificant change in the cerebellum and brainstem brain regions.3. XFM-specific narcotic antagonist was given by intraperitoneal injection for anti-anesthesia,the positive expression levels of NMDAR1in cerebral cortex, thalamus, cerebellum significantlydecreased while the positive expression levels of NMDAR1in hippocampus significantlyincreased when compared with control group. The positive expression levels of NMDAR1incerebral cortex, hippocampus, thalamus, cerebellum significantly increased when compared withXFM group. The positive expression of NMDAR1showed no significant change in the brainstembrain regions in the process of anesthesia and anti-anesthesia. 4. XFM-specific narcotic antagonist was given by intraperitoneal injection for anti-anesthesia,the positive expression levels of BDZR in cerebral cortex, hippocampus, thalamus showed nosignificantly change compared with the control group. The positive expression of BDZR decreasedsignificantly in the cerebral cortex, hippocampus, thalamus brain regions compared with P(anesthesia) group.The positive expression of BDZR showed no significant change in thecerebellum and brainstem brain regions.The experimental results showed that:(1) The influence of XFM on NMDAR1positiveexpression level in cerebral cortex, hippocampus, thalamus and cerebellum, and on BDZR positiveexpression level in cerebral cortex, hippocampus, thalamus might be one of the importantmechanisms of XFM for general anesthesia. XFM might reduce NMDAR1positive expressionlevel in cerebral cortex, hippocampus, thalamus and cerebellum brain regions associated with theincrease of BDZR positive expression level in cerebral cortex, hippocampus, thalamus brainregions.(2) The influence of XFM-specific narcotic antagonist on NMDAR1positive expressionlevel in cerebral cortex, hippocampus, thalamus and cerebellum, and on BDZR positive expressionlevel in cerebral cortex, hippocampus, thalamus might be one of the important mechanisms ofXFM-specific narcotic antagonist for anti-anesthesia. XFM-specific narcotic antagonist mightincrease NMDAR1positive expression level in cerebral cortex, hippocampus, hypothalamus brainregions and cerebellum associated with the decrease of BDZR positive expression level in cerebralcortex, hippocampus, thalamus brain regions.