Mechanical injuries to the external regions of the brain including the cerebral cortex and other parts of the telencephalon are common yet relatively untreatable. The predicament in recovery from brain injury is that the adult central nervous system is generally thought to be incapable of replacing dead neurons. As the subventricular zone （SVZ） is now known to be neurogenic and is in close proximity to the cerebral cortex and other functionally important forebrain areas, the neurogeny of SVZ brings hope to the repair of brain injury. Because of the high frequency of injuries to the cerebral cortex and its functional importance in humans, many laboratories have studied the results of unilateral aspiration or percussion injury of the cerebral cortex. However,
Background Activation of N-methyl-D-aspartate （NMDA） receptors and alpha-amino-3-hydroxy-5-methyl- 4-isoxazole-propionic acid （AMPA） receptors play an important role in the neurons death induced by ischemia. The mitigating effect of intravenous anesthetics on ischemic neuron injury is related to their influence on NMDA receptors. This study was performed to investigate the effect of ketamine-midazolam anesthesia on the NMDA and AMPA receptor subunits expression in the peri-infarction of ischemic rat brain and explore its potential mechanism of neuroprotection. Methods Thirty Sprague Dawley （SD） rats were subjected to permanent middle cerebral artery occlusion under ketamine/atropine （100/0.05 mg/kg） or ketamine-midazolam/atropine （60/50/0.05 mg/kg） intraperitoneal anesthesia （n=15 each）. Twenty-four hours after ischemia, five rats in each group were killed by injecting the above dosage of ketamine or ketamine-midazolam intraperitoneally and infarct size was measured. Twenty-four and 72 hours after ischemia, four rats in each group were killed by injecting the above dosage of ketamine or ketamine-midazolam intraperitoneally. After staining the brain tissue slices with toluidine blue, the survived neurons in the peri-infarction were observed. Also, the expression level of NMDA receptors 1 （NR1）, NMDA receptors 2A （NR2A）, NMDA receptors 2B （NR2B） and AMPA （GluR1 subunit） were determined by grayscale analysis in immunohistochemical stained slices. Results Compared with ketamine anesthesia, ketamine-midazolam anesthesia produced not only smaller infarct size [（24.1±4.6）% vs （38.4±4.2）%, P〈0.05], but also higher neuron density （24 hours： 846±16 vs 756±24, P〈0.05; 72 hours： 882±22 vs 785± 18, P〈0.05） and lower NR2A （24 hours： 123.0±4.9 vs 95.0±2.5, P〈 0.05; 72 hours： 77.8±4.1 vs 54.2±3.9, P〈0.05） and NR2B （24 hours： 98.5±2.7 vs 76.3±2.4, P〈0.05; 72 hours： 67.2±7.5 vs 22.2± 2.6, P〈0.05） expression level in the peri-infarct
Objective To investigate the proliferative response and time course of endogenous neural stem/progenitor cells after cerebral cortical concis in the adult rats. Methods Eighty adult male Sprague-Dawley rats were used in this study. Cumulative BrdU labeling was employed to detect the proliferating cells. At 1d, 3d, 7d, 14d, and 21d after cerebral cortical concis, the rats were killed for BrdU immunohistochemical staining and cell counting in the injured ipsilateral SVZ. Results Little BrdU immunoreactivity cells was present in SVZ of the control rats from day 7 to day 21 after sham operation. The number of BrdU immunoreactivity cells in the injured ipsilateral SVZ increased at day 1 and peaked at day 7 after cerebral cortical concis. Conclusion After cerebral cortical concis of the adult rats, neural stem/progenitor cells in the injured ipsilateral SVZ markedly proliferated with a peak at day 7. This finding may be important for manipulating SVZ cells to promote the recovery from cerebral cortical concis.
