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05 January 2013, Volume 8 Issue 1 Previous Issue    Next Issue

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Transferrin receptor and ferritin-H are developmentally regulated in oligodendrocyte lineage cells Yunxia Li, Qiang Guan, Yuhui Chen, Hongjie Han, Wuchao Liu, Zhiyu Nie 2013, 8 (1):  6-12.  doi: 10.3969/j.issn.1673-5374.2013.01.001 Abstract ( 457 )   PDF (191KB) ( 1184 )   Save Iron is an essential trophic element that is required for cell viability and differentiation, especially in oligodendrocytes, which consume relatively high rates of energy to produce myelin. Multiple iron metabolism proteins are expressed in the brain including transferrin receptor and ferritin-H. However, it is still unknown whether they are developmentally regulated in oligodendrocyte lineage cells for myelination. Here, using an in vitro cultured differentiation model of oligodendrocytes, we found that both transferrin receptor and ferritin-H are significantly upregulated during oligodendrocyte maturation, implying the essential role of iron in the development of oligodendrocytes. Additional different doses of Fe3+ in the cultured medium did not affect oligodendrocyte precursor cell maturation or ferritin-H expression but decreased the expression of the transferrin receptor. These results indicate that upregulation of both transferrin receptor and ferritin-H contributes to maturation and myelination of oligodendrocyte precursor cells. References | Related Articles | Metrics

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Features of adult neurogenesis and neurochemical signaling in the Cherry salmon Oncorhynchus masou brain Evgeniya V. Pushchina, Dmitry K. Оbukhov, Anatoly A. Varaksin 2013, 8 (1):  13-23.  doi: 10.3969/j.issn.1673-5374.2013.01.002 Abstract ( 335 )   PDF (461KB) ( 823 )   Save We investigated the distribution of gamma aminobutyric acid, tyrosine hydroxylase and nitric oxide-producing elements in a cherry salmon Oncorhynchus masou brain at various stages of postnatal ontogenesis by immunohistochemical staining and histochemical staining. The periventricular region cells exhibited the morphology of neurons and glia including radial glia-like cells and contained several neurochemical substances. Heterogeneous populations of tyrosine hydroxylase-, gamma aminobutyric acid-immunoreactive, аs well as nicotinamide adenine dinucleotide phosphate diaphorase-positive cells were observed in proliferating cell nuclear antigen-immunoreactive proliferative zones in periventricular area of diencephalon, central grey layer of dorsomedial tegmentum, medulla and spinal cord. Immunolocalization of Pax6 in the cherry salmon brain revealed a neuromeric construction of the brain at various stages of postnatal ontogenesis, and this was confirmed by tyrosine hydroxylase and gamma aminobutyric acid labeling. References | Related Articles | Metrics

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A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development Zhixing Ma, Qingyu Li, Zhengyu Zhang, Yufang Zheng 2013, 8 (1):  24-30.  doi: 10.3969/j.issn.1673-5374.2013.01.003 Abstract ( 265 )   PDF (345KB) ( 804 )   Save The multiple-layer structure of the cerebral cortex is important for its functions. Such a structure is generated based on the proliferation and differentiation of neural stem/progenitor cells. Notch functions as a molecular switch for neural stem/progenitor cell fate during cortex development but the mechanism remains unclear. Biochemical and cellular studies showed that Notch receptor activation induces several proteases to release the Notch intracellular domain (NICD). A Disintegrin and Metalloprotease 10 (ADAM10) might be a physiological rate-limiting S2 enzyme for Notch activation. Nestin-driven conditional ADAM10 knockout in mouse cortex showed that ADAM10 is critical for maintenance of the neural stem cell population during early embryonic cortex development. However, the expression pattern and function of ADAM10 during later cerebral cortex development remains poorly understood. We performed in situ hybridization for ADAM10 mRNA and immunofluorescent analysis to determine the expression of ADAM10 and NICD in mouse cortex from embryonic day 9 (E14.5) to postnatal day 1 (P1). ADAM10 and NICD were highly co-localized in the cortex of E16.5 to P1 mice. Comparisons of expression patterns of ADAM10 with Nestin (neural stem cell marker), Tuj1 (mature neuron marker), and S100β (glia marker) showed that ADAM10 expression highly matched that of S100β and partially matched that of Tuj1 at later embryonic to early postnatal cortex developmental stages. Such expression patterns indicated that ADAM10-Notch signaling might have a critical function in neuronal maturation and gliogenesis during cortex development. References | Related Articles | Metrics

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Multi-porous electroactive poly(L-lactic acid)/ polypyrrole composite micro/nano fibrous scaffolds promote neurite outgrowth in PC12 cells Qiaozhen Yu, Shuiling Xu, Kuihua Zhang, Yongming Shan 2013, 8 (1):  31-38.  doi: 10.3969/j.issn.1673-5374.2013.01.004 Abstract ( 314 )   PDF (324KB) ( 948 )   Save In this study, poly(L-lactic acid)/ammonium persulfate doped-polypyrrole composite fibrous scaffolds with moderate conductivity were produced by combining electrospinning with in situ polymerization. PC12 cells were cultured on these fibrous scaffolds and their growth following electrical stimulation (0–20.0 µA stimulus intensity, for 1–4 days) was observed using inverted light microscopy, and scanning electron microscopy coupled with the MTT cell viability test. The results demonstrated that the poly(L-lactic acid)/ammonium persulfate doped-polypyrrole fibrous scaffold was a dual multi-porous micro/nano fibrous scaffold. An electrical stimulation with a current intensity 5.0–   10.0 µA for about 2 days enhanced neuronal growth and neurite outgrowth, while a high current intensity (over 15.0 µA) suppressed them. These results indicate that electrical stimulation with a moderate current intensity for an optimum time frame can promote neuronal growth and neurite outgrowth in an intensity- and time-dependent manner. References | Related Articles | Metrics

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The novel amyloid-beta peptide aptamer inhibits intracellular amyloid-beta peptide toxicity Xu Wang, Yi Yang, Mingyue Jia, Chi Ma, Mingyu Wang, Lihe Che, Yu Yang, Jiang Wu 2013, 8 (1):  39-48.  doi: 10.3969/j.issn.1673-5374.2013.01.005 Abstract ( 174 )   PDF (599KB) ( 1739 )   Save Amyloid β peptide binding alcohol dehydrogenase (ABAD) decoy peptide (DP) can competitively antagonize binding of amyloid β peptide to ABAD and inhibit the cytotoxic effects of amyloid β peptide. Based on peptide aptamers, the present study inserted ABAD-DP into the disulfide bond of human thioredoxin (TRX) using molecular cloning technique to construct a fusion gene that can express the TRX1-ABAD-DP-TRX2 aptamer. Moreover, adeno-associated virus was used to allow its stable expression. Immunofluorescent staining revealed the co-expression of the transduced fusion gene TRX1-ABAD-DP-TRX2 and amyloid β peptide in NIH-3T3 cells, indicating that the TRX1-ABAD-DP-TRX2 aptamer can bind amyloid β peptide within cells. In addition, cell morphology and MTT results suggested that TRX1-ABAD-DP-TRX2 attenuated amyloid β peptide-induced SH-SY5Y cell injury and improved cell viability. These findings confirmed the possibility of constructing TRX-based peptide aptamer using ABAD-DP. Moreover, TRX1-ABAD-DP-TRX2 inhibited the cytotoxic effect of amyloid β peptide. References | Related Articles | Metrics

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Chronic pre-treatment with memantine prevents amyloid-beta protein-mediated long-term potentiation disruption Fushun Li, Xiaowei Chen, Feiming Wang, Shujun Xu, Lan Chang, Roger Anwyl, Qinwen Wang 2013, 8 (1):  49-55.  doi: 10.3969/j.issn.1673-5374.2013.01.006 Abstract ( 305 )   PDF (284KB) ( 1040 )   Save Previous studies indicate that memantine, a low-affinity N-methyl-D-aspartate receptor antagonist, exerted acute protective effects against amyloid-β protein-induced neurotoxicity. In the present study, the chronic effects and mechanisms of memantine were investigated further using electrophysiological methods. The results showed that 7-day intraperitoneal application of memantine, at doses of 5 mg/kg or 20 mg/kg, did not alter hippocampal long-term potentiation induction in rats, while 40 mg/kg memantine presented potent long-term potentiation inhibition. Then further in vitro studys were carried out in 5 mg/kg and 20 mg/kg memantine treated rats. We found that 20 mg/kg memantine attenuated the potent long-term potentiation inhibition caused by exposure to amyloid-β protein in the dentate gyrus in vitro. These findings are the first to demonstrate the antagonizing effect of long-term systematic treatment of memantine against amyloid-β protein triggered long-term potentiation inhibition to improve synaptic plasticity. References | Related Articles | Metrics

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Regulation of adenosine triphosphate-sensitive potassium channels suppresses the toxic effects of amyloid-beta peptide (25–35) Min Kong, Maowen Ba, Hui Liang, Peng Shao, Tianxia Yu, Ying Wang 2013, 8 (1):  56-63.  doi: 10.3969/j.issn.1673-5374.2013.01.007 Abstract ( 282 )   PDF (242KB) ( 793 )   Save In this study, we treated PC12 cells with 0–20 µM amyloid-β peptide (25–35) for 24 hours to induce cytotoxicity, and found that 5–20 µM amyloid-β peptide (25–35) decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide (25–35). Diazoxide protected PC12 cells against amyloid-β peptide (25–35)-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nω-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide (25–35)-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H2O2-degrading enzyme catalase could not reverse the amyloid-β peptide (25–35)-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-β peptide (25–35) did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide (25–35) cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide (25–35). References | Related Articles | Metrics

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Expression of netrin-1 and its receptors, deleted in colorectal cancer and uncoordinated locomotion-5 homolog B, in rat brain following focal cerebral ischemia reperfusion injury Xiaodan Wang, Jinming Xu, Jieqin Gong, Hui Shen, Xiaoping Wang 2013, 8 (1):  64-69.  doi: 10.3969/j.issn.1673-5374.2013.01.008 Abstract ( 225 )   PDF (279KB) ( 1165 )   Save Netrin-1 is currently one of the most highly studied axon guidance factors. Netrin-1 is widely expressed in the embryonic central nervous system, and together with the deleted in colorectal cancer and uncoordinated locomotion-5 homolog B receptors, netrin-1 plays a guiding role in the construction of neural conduction pathways and the directional migration of neuronal cells. In this study, we established a rat middle cerebral artery ischemia reperfusion model using the intraluminal thread technique. Immunofluorescence microscopy showed that the expression of netrin-1 and deleted in colorectal cancer in the ischemic penumbra was upregulated at 1 day after reperfusion, reached a peak at 14 days, and decreased at 21 days. There was no obvious change in the expression of uncoordinated locomotion-5 homolog B during this time period. Double immunofluorescence labeling revealed that netrin-1 was expressed in neuronal cells and around small vessels, but not in astrocytes and microglia, while deleted in colorectal cancer was localized in the cell membranes and protrusions of neurons and astrocytes. Our experimental findings indicate that netrin-1 may be involved in post-ischemic repair and neuronal protection via deleted in colorectal cancer receptors. References | Related Articles | Metrics

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Involvement of the Wnt signaling pathway and cell apoptosis in the rat hippocampus following cerebral ischemia/reperfusion injury Bin Liu, Jing Tang, Shiying Li, Yuqin Zhang, Yan Li, Xiaoliu Dong 2013, 8 (1):  70-75.  doi: 10.3969/j.issn.1673-5374.2013.01.009 Abstract ( 227 )   PDF (296KB) ( 780 )   Save We investigated the role of the Wnt signaling pathway in cerebral ischemia/reperfusion injury by examining β-catenin and glycogen synthase kinase-3β protein expression in the rat hippocampal CA1 region following acute cerebral ischemia/reperfusion. Our results demonstrate that cell apoptosis increases in the CA1 region following ischemia/reperfusion. In addition, β-catenin and glycogen synthase kinase-3β protein expression gradually increases, peaking at 48 hours following reperfusion. Dickkopf-1 administration, after cerebral ischemia/reperfusion injury, results in decreased cell apoptosis, and β-catenin and glycogen synthase kinase-3β expression, in the CA1 region. This suggests that β-catenin and glycogen synthase kinase-3β, both components of the Wnt signaling pathway, participate in cell apoptosis following cerebral ischemia/reperfusion injury. References | Related Articles | Metrics

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Changes in secretory pathway Ca2+ -ATPase 2 following focal cerebral ischemia/reperfusion injury Tonglin Lu, Zhiping Hu, Liuwang Zeng, Zheng Jiang 2013, 8 (1):  76-82.  doi: 10.3969/j.issn.1673-5374.2013.01.010 Abstract ( 562 )   PDF (171KB) ( 868 )   Save This study aimed to investigate changes in secretory pathway Ca2+ -ATPase 2 expression following cerebral ischemia/reperfusion injury, and to define the role of Ca2+ -ATPases in oxidative stress. A rat model of cerebral ischemia/reperfusion injury was established using the unilateral middle cerebral artery occlusion method. Immunohistochemistry and reverse transcription-PCR assay results showed that compared with the control group, the expression of secretory pathway Ca2+ -ATPase 2 protein and mRNA in the cerebral cortex and hippocampus of male rats did not significantly change during the ischemic period. However, secretory pathway Ca2+ -ATPase 2 protein and mRNA expression reduced gradually at 1, 3, and 24 hours during the reperfusion period. Our experimental findings indicate that levels of secretory pathway Ca2+ -ATPase 2 protein and mRNA expression in brain tissue change in response to cerebral ischemia/reperfusion injury. References | Related Articles | Metrics

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Dynamic changes in proprotein convertase 2 activity in cortical neurons after ischemia/reperfusion and oxygen-glucose deprivation Shuqin Zhan, An Zhou, Chelsea Piper, Tao Yang 2013, 8 (1):  83-89.  doi: 10.3969/j.issn.1673-5374.2013.01.011 Abstract ( 275 )   PDF (152KB) ( 951 )   Save In this study, a rat model of transient focal cerebral ischemia was established by performing     100 minutes of middle cerebral artery occlusion, and an in vitro model of experimental oxygen-glucose deprivation using cultured rat cortical neurons was established. Proprotein convertase 2 activity gradually decreased in the ischemic cortex with increasing duration of reperfusion. In cultured rat cortical neurons, the number of terminal deoxynucleotidyl transferase-mediated 2’-deoxyuridine 5’-triphosphate-biotin nick end labeling-positive neurons significantly increased and proprotein convertase 2 activity also decreased gradually with increasing duration of oxygen-glucose deprivation. These experimental findings indicate that proprotein convertase 2 activity decreases in ischemic rat cortex after reperfusion, as well as in cultured rat cortical neurons after oxygen-glucose deprivation. These changes in enzyme activity may play an important pathological role in brain injury. References | Related Articles | Metrics

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Motor recovery via aberrant pyramidal tract in a patient with traumatic brain injuryA diffusion tensor tractography study Sang Seok Yeo, Sung Ho Jang 2013, 8 (1):  90-94.  doi: 10.3969/j.issn.1673-5374.2013.01.012 Abstract ( 294 )   PDF (177KB) ( 901 )   Save The aberrant pyramidal tract is the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem. A 21-year-old man presented with right hemiparesis due to a traumatic intracerebral hemorrhage in the left corona radiata. His motor function recovered almost to the normal state at 10 months after onset. Through diffusion tensor tractography, the pyramidal tract in the affected (left) hemisphere showed discontinuation at the pontine level at 13 months after onset. An aberrant pyramidal tract was observed, which originated from the primary motor cortex and the supplementary motor area and descended through the corona radiata, then through the posterior limb of the internal capsule and the medial lemniscus pathway from the midbrain to the pons, finally entered into the pyramidal tract area at the pontomedullary junction. It suggests that the motor functions of the right extremities in this patient had recovered by this aberrant pyramidal tract. References | Related Articles | Metrics