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    12 June 2014, Volume 9 Issue 11 Previous Issue    Next Issue
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    Current advances in neurotrauma research: diagnosis, neuroprotection, and neurorepair
    Jinhui Chen, Riyi Shi
    2014, 9 (11):  1093-1095.  doi: 10.4103/1673-5374.135306
    Abstract ( 230 )   PDF (152KB) ( 811 )   Save
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    The potential of stem cell-based therapy for retinal repair
    Honghua Yu, Lin Cheng, Kin-Sang Cho
    2014, 9 (11):  1100-1103.  doi: 10.4103/1673-5374.135311
    Abstract ( 399 )   PDF (184KB) ( 670 )   Save

    Retinal degeneration has been known to be caused by genetic mutation, trauma or infection that will lead to irreversible neuronal loss and even blindness. Other than these factors, environmental influences such as ultraviolet radiation and oxidative stress could also bring forth retinal degeneration. Glaucoma, optic neuritis and post-traumatic optic injury are the common retinal diseases leading to degeneration of retinal ganglion cells (RGCs) and their axons. To achieve the goal of stem cell-based therapy, the survival and integration of transplanted cells are critical. Dr. Kin-Sang Cho from Harvard Medical School in USA suggests that to evaluate the potential of stem cell therapy for neurodegenerative disease in central nervous system, retina may be a good choice to be considered because it is an easily accessible organ. In addition, the cornea clarity makes possible for longitudinal imaging the transplanted cells and measuring the retinal function by non-invasive approaches. In contrast to the complex retinal structure, analyze the integration and functional connection of transplanted cells to the host cells in the spinal cord could be simpler.

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    Repair and regeneration properties of Ginkgo biloba after ischemic brain injury
    Aparna Raghavan, Zahoor A. Shah
    2014, 9 (11):  1104-1107.  doi: 10.4103/1673-5374.135308
    Abstract ( 222 )   PDF (538KB) ( 889 )   Save

    Ginkgo Biloba (G. biloba) is a widely studied herb for the treatment of neurological disorders, its use as a symptomatic treatment for dementia has been established in clinical trials. However, its use for the treatment of ischemic stroke in the clinic is still equivocal. EGb 761-treated mice not only showed an increase in the number of NSCs post-stroke, but the majority of them were found in the proximity of the injury site or penumbra area. EGb 761 also enhanced the expression of Wnt, the ligand that is responsible for triggering the canonical Wnt pathway or the Wnt/β-catenin pathway, which constitutes one of the primary signaling mechanisms overseeing endogenous neurogenesis. Thus, EGb 761 can offer a diverse trove of potential drug leads that could someday change the way we think of nerve regeneration and the use of complementary and alternative medicine.

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    Diffusional kurtosis imaging: a promising technique for detecting microstructural changes in neural development and regeneration
    Amir Paydar
    2014, 9 (11):  1108-1109.  doi: 10.4103/1673-5374.135309
    Abstract ( 243 )   PDF (778KB) ( 1274 )   Save

    Brain development is one of the most fascinating subjects in the field of biological sciences. Nonetheless, our scientific community still faces challenges in trying to understand the concepts that define the underlying mechanisms of neural tissue development. After all, it is a very complex subject to grasp and many of the processes that take place during central nervous system maturation are yet to be ascertained. Dr. Amir Paydar from New York University in USA considered that despite this challenge, we have come to recognize that understanding the natural course of normal brain tissue development on both microscopic and macroscopic scales is the key to deciphering the mechanisms through which these neural networks also heal and regenerate. Realizing this concept, they implemented a Magnetic Resonance Imaging (MRI) diffusion technique called Diffusional Kurtosis Imaging (DKI) to investigate the microstructural changes that occur in both the white matter (WM) and gray matter (GM) in the developing brain. But what is the relevance of this discovery for neural regeneration research? The answer to this question is clear. The diffusion barriers which may form due to the progressive increase in macromolecular reorganization during neural maturation are probably similar to ones that take shape during the course of neural regeneration. These barriers may partly result from many cytoarchitectural changes that take place at the microstructural level during both neural development and regeneration. For example, these changes may include the overall increase in the complexity of intrinsic cellular processes (e.g., proliferation of cell membranes, organelles, and extracellular matrix), axonal pruning and cell packing, myelination and functional reorganization of myelin, as well as addition of basal dendrites and transition of radial glial cells to astrocytic neuropil.

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    Methylation reactions at dopaminergic nerve endings, serving as biological off-switches in managing dopaminergic functions
    Clivel G. Charlton
    2014, 9 (11):  1110-1111.  doi: 10.4103/1673-5374.135310
    Abstract ( 323 )   PDF (134KB) ( 675 )   Save

    Synaptic dopamine (DA) controls complex and specialized functions including, movements, behavior, mood, perception, reward, and more recently, neurogenesisand neuroregeneration. The methylation of DA receptor protein is a stable phenomenon that may serve to progressively down-regulate DA synaptic activity, causing age-related decline in movements. Prof. Clivel G. Charlton , who comes from Meharry Medical College in USA ties this perspective together long-established findings, recent discoveries and a hypothesis to show that methylation, along with the standard release and uptake processes for DA, may help to explain the fidelity by which the functions that DA controls are regulated. Accepting the role of methylation in the synaptic activity of DA may lead to better ways of managing disorders related to DA synaptic functions. Moreover, the finding that DA depletion impairs precursor cell proliferation in PD corresponds with reports that DA promotes neurogenesis and neuroregeneration. The multiple-switch-concept in the regulation of DA synaptic functions is novel, requires further investigation.

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    Melatonin reduces traumatic brain injury-induced oxidative stress in the cerebral cortex and blood of rats
    Nilgün Şenol, Mustafa Nazıroğlu
    2014, 9 (11):  1112-1116.  doi: 10.4103/1673-5374.135312
    Abstract ( 279 )   PDF (219KB) ( 849 )   Save

    Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We investigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex  β-carotene, vitamin C, vitamin E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain injury-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.

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    Neuroprotective effect of ischemic preconditioning in focal cerebral infarction: relationship with upregulation of vascular endothelial growth factor
    Yong Liu, Suiqiang Zhu, Yunfu Wang, Jingquan Hu, Lili Xu, Li Ding, Guangjian Liu
    2014, 9 (11):  1117-1121.  doi: 10.4103/1673-5374.135313
    Abstract ( 275 )   PDF (270KB) ( 944 )   Save

    Neuroprotection by ischemic preconditioning has been confirmed by many studies, but the precise mechanism remains unclear. In the present study, we performed cerebral ischemic preconditioning in rats by simulating a transient ischemic attack twice (each a 20-minute occlusion of the middle cerebral artery) before inducing focal cerebral infarction (2 hour occlusion-reperfusion in the same artery). We also explored the mechanism underlying the neuroprotective effect of ischemic preconditioning. Seven days after occlusion-reperfusion, tetrazolium chloride staining and immunohistochemistry revealed that the infarct volume was significantly smaller in the group that underwent preconditioning than in the model group. Furthermore, vascular endothelial growth factor immunoreactivity was considerably greater in the hippocampal CA3 region of preconditioned rats than model rats. Our results suggest that the protective effects of ischemic preconditioning on focal cerebral infarction are associated with upregulation of vascular endothelial growth factor.

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    Potential targets for protecting against hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats
    Xiangyu Ji, Li’na Zhang, Ran Liu, Yingzhi Liu, Jianfang Song, He Dong, Yanfang Jia, Zangong Zhou
    2014, 9 (11):  1122-1128.  doi: 10.4103/1673-5374.135314
    Abstract ( 221 )   PDF (1057KB) ( 915 )   Save

    Mitochondria play an important role in neuronal apoptosis caused by cerebral ischemia, and the role is mediated by the expression of mitochondrial proteins. This study investigated the involvement of mitochondrial proteins in hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats using a comparative proteomics strategy. Our experimental results show that the aged rat brain is sensitive to ischemia-reperfusion injury and that transient ischemia led to cell apoptosis in the hippocampus and changes in memory and cognition of aged rats. Differential proteomics analysis suggested that this phenomenon may be mediated by mitochondrial proteins associated with energy metabolism and apoptosis in aged rats. This study provides potential drug targets for the treatment of transient cerebral ischemia-reperfusion injury.

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    Heavy ion and X-ray irradiation alter the cytoskeleton and cytomechanics of cortical neurons
    Yuting Du, Jie Zhang, Qian Zheng, Mingxin Li, Yang Liu, Baoping Zhang, Bin Liu, Hong Zhang, Guoying Miao
    2014, 9 (11):  1129-1137.  doi: 10.4103/1673-5374.135315
    Abstract ( 314 )   PDF (3129KB) ( 1125 )   Save

    Heavy ion beams with high linear energy transfer exhibit more beneficial physical and biological performance than conventional X-rays, thus improving the potential of this type of radiotherapy in the treatment of cancer. However, these two radiotherapy modalities both cause inevitable brain injury. The objective of this study was to evaluate the effects of heavy ion and X-ray irradiation on the cytoskeleton and cytomechanical properties of rat cortical neurons, as well as to determine the potential mechanism of neuronal injury after irradiation. Cortical neurons from 30 new-born mice were irradiated with heavy ion beams at a single dose of 2 Gy and X-rays at a single dose of 4 Gy; subsequent evaluation of their effects were carried out at 24 hours after irradiation. An immunofluorescence assay showed that after irradiation with both the heavy ion beam and X-rays, the number of primary neurons was significantly decreased, and there was evidence of apoptosis. Radiation-induced neuronal injury was more apparent after X-irradiation. Under atomic force microscopy, the neuronal membrane appeared rough and neuronal rigidity had increased. These cell changes were more apparent following exposure to X-rays. Our findings indicated that damage caused by heavy ion and X-ray irradiation resulted in the structural distortion and rearrangement of the cytoskeleton, and affected the cytomechanical properties of the cortical neurons. Moreover, this radiation injury to normal neurons was much severer after irradiation with X-rays than after heavy ion beam irradiation.

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    Somatosensory stimulation suppresses the excitability of pyramidal cells in the hippocampal CA1 region in rats
    Yang Wang, Zhouyan Feng, Jing Wang, Xiaojing Zheng
    2014, 9 (11):  1138-1144.  doi: 10.4103/1673-5374.135316
    Abstract ( 160 )   PDF (568KB) ( 753 )   Save

    The hippocampal region of the brain is important for encoding environment inputs and memory formation. However, the underlying mechanisms are unclear. To investigate the behavior of individual neurons in response to somatosensory inputs in the hippocampal CA1 region, we recorded and analyzed changes in local field potentials and the firing rates of individual pyramidal cells and interneurons during tail clamping in urethane-anesthetized rats. We also explored the mechanisms underlying the neuronal responses. Somatosensory stimulation, in the form of tail clamping, chan-ged local field potentials into theta rhythm-dominated waveforms, decreased the spike firing of pyramidal cells, and increased interneuron firing. In addition, somatosensory stimulation attenuated orthodromic-evoked population spikes. These results suggest that somatosensory stimulation suppresses the excitability of pyramidal cells in the hippocampal CA1 region. Increased inhibition by local interneurons might underlie this effect. These findings provide insight into the mechanisms of signal processing in the hippocampus and suggest that sensory stimulation might have therapeutic potential for brain disorders associated with neuronal hyperexcitability.

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    A viral vector expressing hypoxia-inducible factor 1 alpha inhibits hippocampal neuronal apoptosis
    Xiqing Chai, Weina Kong, Lingyun Liu, Wenguo Yu, Zhenqing Zhang, Yimin Sun
    2014, 9 (11):  1145-1153.  doi: 10.4103/1673-5374.135317
    Abstract ( 212 )   PDF (2058KB) ( 751 )   Save

    Hypoxia-inducible factor 1 (HIF-1) attenuates amyloid-beta protein neurotoxicity and decreases apoptosis induced by oxidative stress or hypoxia in cortical neurons. In this study, we constructed a recombinant adeno-associated virus (rAAV) vector expressing the human HIF-1α gene (rAAV-HIF-1α), and tested the assumption that rAAV-HIF-1α represses hippocampal neuronal apoptosis induced by amyloid-beta protein. Our results confirmed that rAAV-HIF-1α significantly reduces apoptosis induced by amyloid-beta protein in primary cultured hippocampal neurons. Direct intracerebral rAAV-HIF-1α administration also induced robust and prolonged HIF-1α production in rat hippocampus. Single rAAV-HIF-1α administration resulted in decreased apoptosis of hippocampal neurons in an Alzheimer’s disease rat model established by intracerebroventricular injection of aggregated amyloid-beta protein (25–35). Our in vitro and in vivo findings demonstrate that HIF-1 has potential for attenuating hippocampal neuronal apoptosis induced by amyloid-beta protein, and provides experimental support for treatment of neurodegenerative diseases using gene therapy.

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    High matrix metalloproteinase-9 expression induces angiogenesis and basement membrane degradation in stroke-prone spontaneously hypertensive rats after cerebral infarction
    Huilian Hou, Guanjun Zhang, Hongyan Wang, Huilin Gong, Chunbao Wang, Xuebin Zhang
    2014, 9 (11):  1154-1162.  doi: 10.4103/1673-5374.135318
    Abstract ( 175 )   PDF (2267KB) ( 808 )   Save

    Basement membrane degradation and blood-brain barrier damage appear after cerebral infarction, severely impacting neuronal and brain functioning; however, the underlying pathogenetic mechanisms remain poorly understood. In this study, we induced cerebral infarction in stroke-prone spontaneously hypertensive rats by intragastric administration of high-sodium water (1.3% NaCl) for 7 consecutive weeks. Immunohistochemical and immunofluorescence assays demonstrated that, compared with the non-infarcted contralateral hemisphere, stroke-prone spontaneously hypertensive rats on normal sodium intake and Wistar-Kyoto rats, matrix metalloproteinase-9 expression, the number of blood vessels with discontinuous collagen IV expression and microvessel density were significantly higher, and the number of continuous collagen IV-positive blood vessels was lower in the infarct border zones of stroke-prone spontaneously hypertensive rats given high-sodium water. Linear correlation analysis showed matrix metalloproteinase-9 expression was positively correlated with the number of discontinuously collagen IV-labeled blood vessels and microvessel density in cerebral infarcts of stroke-prone spontaneously hypertensive rats. These results suggest that matrix metalloproteinase-9 upregulation is associated with increased regional angiogenesis and degradation of collagen IV, the major component of the basal lamina, in stroke-prone spontaneously hypertensive rats with high-sodium water-induced focal cerebral infarction.

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    Acupuncture at the Taixi (KI3) acupoint activates cerebral neurons in elderly patients with mild cognitive impairment
    Shangjie Chen, Maosheng Xu, Hong Li, Jiuping Liang, Liang Yin, Xia Liu, Xinyan Jia, Fen Zhu, Dan Wang, Xuemin Shi, Lihua Zhao
    2014, 9 (11):  1163-1168.  doi: 10.4103/1673-5374.135319
    Abstract ( 271 )   PDF (285KB) ( 901 )   Save

    Our previous findings have demonstrated that acupuncture at the Taixi (KI3) acupoint in healthy youths can activate neurons in cognitive-related cerebral cortex. Here, we investigated whether acupuncture at this acupoint in elderly patients with mild cognitive impairment can also activate neurons in these regions. Resting state and task-related functional magnetic resonance imaging showed that the pinprick senstation of acupuncture at the Taixi acupoint differed significantly between elderly patients with mild cognitive impairment and healthy elderly controls. Results showed that 20 brain regions were activated in both groups of participants, including the bilateral anterior cingulate gyrus (Brodmann areas [BA] 32, 24), left medial frontal cortex (BA 9, 10, 11), left cuneus (BA 19), left middle frontal gyrus (BA 11), left lingual gyrus (BA 18), right medial frontal gyrus (BA 11), bilateral inferior frontal gyrus (BA 47), left superior frontal gyrus (BA11), right cuneus (BA 19, 18), right superior temporal gyrus (BA 38), left subcallosal gyrus (BA 47), bilateral precuneus (BA 19), right medial frontal gyrus (BA 10), right superior frontal (BA 11), left cingulate gyrus (BA 32), left precentral gyrus (BA 6), and right fusiform gyrus (BA 19). These results suggest that acupuncture at the Taixi acupoint in elderly patients with mild cognitive impairment can also activate some brain regions.

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