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Am J Emerg Med. 2013 Feb;31(2):353-9. doi: 10.1016/j.ajem.2012.08.039. Epub 2012 Nov 15.

Changes in expression of Nogo receptor 1 in hippocampus and cortex after cardiopulmonary resuscitation in rats.

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Department of Emergency, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, People's Republic of China.


The aim of this study was to investigate changes in Nogo receptor 1 (NgR(1)) expression in the cerebrum after cardiopulmonary resuscitation (CPR) in rats. Cardiac arrest was induced by alternating current in 50 SD rats through transcutaneous electrical epicardium stimulation, and CPR was performed with the Utstein mode 6 minutes after cardiac arrest. Rats were killed 1, 3, and 7 days after CPR. We performed immunofluorescence with antibodies against NgR(1) to map the distribution of NgR(1) in the rat cerebrum, whereas quantitative polymerase chain reaction was performed for quantitative analysis of NgR(1) messenger RNA (mRNA). There was a striking transient up-regulation of the NgR(1) protein and mRNA in both the hippocampus and cortex in response to CPR. Nogo receptor 1 proteins were strongly expressed in hippocampal neurons 1 and 3 days after CPR (P < .001 for 1 day and P < .05 for 3 days, vs the control group, respectively), which returned to the basal level 7 days after CPR. In the cortex, staining moderately increased 1 day after CPR and got the peak level after 3 days (P < .001), returning to normal expression levels on day 7. The levels of NgR(1) mRNA in the hippocampus and cerebral cortical cortex showed the same trend with staining. The changes were significantly different between day 3 and baseline in both the hippocampus and cortex (P < .05, respectively). Furthermore, there were significant differences between the hippocampus and cerebral cortical cortex at 1 day and 3 days after the CPR (P < .05, respectively). There was a transient increase in NgR(1) in the vulnerable areas of the rat brain after CPR. Blockade of NgR(1) may be important in maintaining the high regenerative capacity of neurons during the time window when NgR(1) expression increases.

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