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• W2361184927 abstract "Mechanical injuries to the external regions of the brain including the cerebral cortex and other parts of the telencephalon are common yet relatively untreatable.1 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.2,3 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.4-6 However, little is known about the response of endogenous neural stem/progenitor cells following loss of the cerebral cortex that commonly occurred in the neurosurgery. We have characterized the time course of the proliferation of neural stem/progenitor cells in the SVZ in brain to loss of cortical cells. METHODS Experimental animals Eighty male Sprague-Dawley rats weighing 300 g to 350 g, provided by the Centre of Experimental Animals, School of Medicine, Xi'an Jiaotong University, were used in this study. After one week acclimatisation in the laboratory, the rats were anesthetized by intraperitoneal injection of 40 mg/kg 1% pentobarbital sodium (10 mg/ml, Sigma-Aldrich, USA) and then underwent cortical excision. Cerebral cortical excision model The rats were fixed on stereotaxic apparatus after anaesthesia. The skin was incised and the periosteum separated. A 4.0 mm×4.0 mm window whose centre located at 0.0 mm posterior to and 4.0 mm lateral to the bregma was made in the cranium according to the stereotaxic atlas of rat brain by Jeoje Paxinos and CharlesWatson as well as the method reported by Tang et al (Chin J Neuroanatomy 1994; 10: 213-218). A block of cerebral cortex (3 mm×3 mm×1 mm) was removed through the window. Rats in the control group underwent the same procedure except that the block of cerebral cortex was not removed. BrdU administration and tissue preparation To demonstrate subventricular zone cell, proliferation after cerebral cortical excision, the BrdU labelling method reported by Zhang et al (Neurosci 2001; 105: 33-41) was adopted in this experiment. In brief, BrdU (Sigma-Aldrich, USA) was dissolved in normal saline (10 mg/ml) and injected intraperitoneally (50 mg/kg) at the time of excision and then daily for 13 consecutive days. On day 1, 3, 7, 14 and 21 after cerebral cortical excision, 5 rats were anesthetized and perfused transcardially with heparinized normal saline followed by 4% paraformaldehyde in PBS (pH 7.4). The rats in the control group received the same dose of BrdU injection and 5 were sacrificed at each of the corresponding time points. The brain tissue between +0.2 mm and -1.2 mm from the bregma was taken to prepare 20 μm frozen coronal sections in a similar manner (HM505 E, Zeiss, Germany), which underwent HE or immunohistochemical staining. Immunohistochemistry Three sections, spaced 200 μm apart, from each rat were used for BrdU immunohistochemical staining. The sections were treated with 50% formamide 2× SSC at 65°C for 2 hours, incubated in 2 mol/L HCl for 30 minutes at 37°C to denature the DNA, and then rinsed in 0.1 mol/L boric acid (pH 8.5) at room temperature for 10 minutes. The sections were incubated in 1% H2O2 and PBS for 20 minutes, in blocking solution (2% goat serum, 0.3% Triton X-100 and 0.1% bovine serum albumin in PBS) for 30 minutes at room temperature before being treated overnight at 4°C with monoclonal mouse anti-BrdU (1:2000, Sigma). Sections were washed with PBS, incubated with biotinylated goat antimouse IgG secondary antibody (Santa Cruz Biotechnology, Santa Cruz, USA; 1:100) for 2 hours at room temperature, washed and placed in avidin- peroxidase conjugate (Santa Cruz, USA) solution for 1 hour. The horseradish peroxidase reaction was detected with 0.05% diaminobenzidine (Boster, China) and 0.03% H2O2. Processing was stopped with H2O and sections were dehydrated through graded alcohols, cleared in xylene and sealed in neutral gum under a coverslip. Sections incubated without mouse monoclonal anti-BrdU antibodies were used negative controls. BrdU positive cell counting BrdU positive cells were counted independently in three immunohistochemically stained coronal sections per animal. The density of BrdU positive cells in the ipsilateral SVZ of injury side was measured according to published methods and expressed as cell number/mm2. Briefly, stained coronal sections were digitized (400 × TCS Sp2 Leica). Three to six fields in the SVZ per rat were analyzed to determine the density of BrdU positive cells. Density of cells within the selected fields was averaged to obtain a mean density value for each animal. Statistical analysis Statistical analysis was made using SPSS 10.0. One way analysis of variance (ANOVA) was followed by post hoc test for multiple comparisons and t test for group comparisons. All values are presented as means±standard error (SE). Statistical significance was set at P<0.05. RESULTS Outcome of experimental rats Five rats of the control group died in the experimental procedure. Besides that, 12 rats of cerebral cortical excision group died in the operation and another before the end of experiment. Cerebral cortical excision HE staining showed profuse erythrocytes and leucocytes in the area around the injured site at day 1 and 3 after cerebral cortical excision. A V-shape cavity was found in the injured cortex at day 7, 14 and 21 after cerebral cortical excision. Additionally, glial scar with different thicknesses was observed at the edge of the V-shape cavity. BrdU immunohistochemistry No positive staining of cell nucleus was observed in the negative control sections (Fig. A). Some BrdU immunoreactive cells were present in SVZ of the control rats from day 7(Fig. B) to day 21 after sham operation. A few BrdU immunoreactivitive cells were found in the injured ipsilateral SVZ at day 1 after excision. More BrdU immunoreactive cells were observed in the injured ipsilateral SVZ at days 3 and 7 (Fig. C) after excision. However, very few BrdU immunoreactive cells existed in the injured ipsilateral SVZ at days 14 and 21 (Fig. D) after excision. Density analysis of BrdU immunoreactivitive cells showed that the number of BrdU immunoreactive cells in the injured ipsilateral SVZ increased during day 1 and was higher again at day 7 after cerebral cortical excision. The density of BrdU immunoreactive cells in the injured ipsilateral SVZ at different times after excision is listed in Table.Fig.: Representative photographs of BrdU immunohistochemical staining (SABC×200). A: The negative control section. B: The normal control at day 7. C and D: BrdU immunoreactive cells in the injured ipsilateral SVZ at day 7 and 14 after cerebral cortical excision, respectively. Box in the photographs indicates the region where BrdU positive cells were counted. LV: Lateral ventricle. CC: Corpus callosum.Table: Density of BrdU immunoreactive cells in SVZ of the brain (mean±SE, cells/mm2)DISCUSSION The adult neural stem cells are multipotential cells with self renewing capacity.7 They are mainly in the subventricular zone of the lateral ventricle wall and dentate gyrus of the hippocampus.8 Under physiological condition, these cells are quiescent or exhibit very limited neurogenesis.8,9 The cellular composition, proliferation, migration and differentiation of SVZ and dentate gyrus have been investigated extensively.10 However, the literature on proliferative response of the adult SVZ cells after mechanical trauma is limited and it is unclear about the response of adult SVZ cells following cerebral cortex excision. In the present study, we found that: 1) cells in the injured ipsilateral SVZ present obvious BrdU immunoreactivity, indicating SVZ cell proliferation after cerebral cortex excision in the adult rats. 2) The number of BrdU immunoreactive cells in the injured ipsilateral SVZ peaks around day 7, suggesting the time window for maximum SVZ cell proliferation being around 7 days after cerebral cortex excision in adult rats. BrdU has been a principal marker for mitotic cells in studies of adult neurogenesis. The substitution of an endogenous DNA base, thymidine, with the BrdU analogue ensures specific labelling of only the dividing cells.11 However, BrdU labels different cell population depending on its administration protocol.12 It has been shown that BrdU labels not only rapidly proliferating cells (probably progenitor cells ) but also slowly dividing cells (putative stem cells) when being administrated daily for consecutive days.13 Based on this BrdU administration protocol, cerebral cortex excision study possibly stimulates mitotic activity of endogenous neural progenitor and stem cells. Recently, some studies determined the proliferative response of progenitor/stem cells in different brain injury models. Szele et al (J Comp Neurol 1996; 368: 439-454) reported that the number of BrdU immunoreactive cells in the SVZ did not change significantly at various times following cortical aspirational lesions. In a rat model, Chirumamilla et al (J Neurotrauma 2002; 19: 693-703) revealed that the number of BrdU labelled SVZ cells increased 2 and 4 days after fluid percussion injury. Jankovski et al14 found that the number of BrdU positive cells in the SVZ/RMS caudal to aspirational lesions of the frontal cortex and olfactory peduncle significantly decreased from 2 days to 7 weeks compared with nonlesioned controls. However, when fluid percussion injury is performed on mice, the numbers of BrdU labelled cells increased in the cerebral cortex and SVZ.15 We found that after cerebral cortical excision in adult rats, the number of BrdU immunoreactive cells in the injured ipsilateral SVZ increased at day 1 and was higher at day 7. Although the time course of SVZ cell proliferation in our experiment is earlier than Chirumamilla's (J Neurotrauma 2002; 19: 693-703) report, it is similar to that found in focal cerebral ischaemic model. The reason for decreased BrdU positive cells in the injured ipsilateral SVZ after day 7 may be due to proliferated cells emigrating from SVZ or dying. These results suggest that different animals differ markedly in their SVZ cell response to some brain injuries. This probably reflects diversity of SVZ cell responses after brain trauma. In conclusion, our findings provide evidence for SVZ cell proliferation and its time course after cerebral cortical excision in the adult rats. Proliferative response of endogenous progenitor/stem cells indicate that the brain attempts to repair its injury although further study is needed to determine whether proliferated cells produce new neurons in the damaged region. In this way, our results may be important for manipulating SVZ cells to promote the recovery from cerebral cortical trauma." @default.
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• W2361184927 date "2006-06-01" @default.
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• W2361184927 title "BrdU-labelled neurons regeneration after cerebral cortex injury in rats" @default.
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