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05 November 2012, Volume 7 Issue 31 Previous Issue    Next Issue

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Relationship of gelatinases-tight junction proteins and blood-brain barrier permeability in the early stage of cerebral ischemia and reperfusion Haolin Xin, Wenzhao Liang, Jing Mang, Lina Lin, Na Guo, Feng Zhang, Zhongxin Xu 2012, 7 (31):  2405-2412.  Abstract ( 251 )   PDF (262KB) ( 963 )   Save Gelatinases matrix metalloproteinase-2 and matrix metalloproteinase-9 have been shown to mediate claudin-5 and occludin degradation, and play an important regulatory role in blood-brain barrier permeability. This study established a rat model of 1.5-hour middle cerebral artery occlusion with reperfusion. Protein expression levels of claudin-5 and occludin gradually decreased in the early stage of reperfusion, which corresponded to the increase of the gelatinolytic activity of matrix metalloproteinase-2 and matrix metalloproteinase-9. In addition, rats that received treatment with matrix metalloproteinase inhibitor N-[(2R)-2-(hydroxamidocarbonylmethyl)-4-methylpenthanoyl]-Ltryptophan methylamide (GM6001) showed a significant reduction in Evans blue leakage and an inhibition of claudin-5 and occludin protein degradation in striatal tissue. These data indicate that matrix metalloproteinase-2 and matrix metalloproteinase-9-mediated claudin-5 and occludin degradation is an important reason for blood-brain barrier leakage in the early stage of reperfusion.The leakage of the blood-brain barrier was present due to gelatinases-mediated degradation of claudin-5 and occludin proteins. We hypothesized that the timely closure of the structural component of the blood-brain barrier (tight junction proteins) is of importance. Related Articles | Metrics

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Activation of hypothalamic gono-like neurons in female rats during estrus Xiaoxuan Ren, Shaojun Wang, Peijing Rong, Bing Zhu 2012, 7 (31):  2413-2423.  Abstract ( 285 )   PDF (318KB) ( 1001 )   Save In mammals, gonadal function is controlled by the activity of hypothalamic gonadotropin-releasing hormone neurons, which control the secretion of adenohypophyseal and gonadal hormones.However, there are a number of unanswered questions in relation to gonadal function. It is currently unknown how erotogenic stimulation of the genitals influences the subpopulation of hypothalamic medial preoptic area neurons, antidromically identified as projecting to the median eminence at different periods of the estrous cycle. Additionally, the distinctiveness of hypothalamic medial preoptic area neurons, with respect to methods of feedback control by exogenous hormones, is also unknown. In this study, spontaneous discharges from individual neurons encountered within the medial preoptic area, gono-like neurons, were recorded extracellularly using glass microelectrodes.To confirm the cellular and histochemical properties of the recording units, antidromic stimulation was performed using a side-by-side bipolar stimulating electrode placed into the median eminence,alongside microiontophoretic injections of the conventional tracer, horseradish peroxidase. In addition, further immunohistochemical analyses were performed. Results showed that elevated gono-neuron activity was accompanied by increased background activity and greater responses to erotogenic stimuli during estrus. Application of clitoral traction stimulation resulted in increased activation of the gono-like neurons. This neuronal activity was noticeably inhibited by β-estradiol administration. Immunohistochemical analyses revealed the presence of gonadotropin-releasing hormone-reactive protein in hypothalamic cells in which electrophysiological recordings were taken.Thus, medial preoptic area neurons represent the subset of hypothalamic gonadotropin-releasing hormone neurons described from brain slices in vitro, and might serve as a useful physiological model to form the basis of future in vivo studies. Related Articles | Metrics

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Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats Hui Zhu, Xiao Han, Dafeng Ji, Guangming Lv, Meiyu Xu 2012, 7 (31):  2424-2431.  Abstract ( 211 )   PDF (208KB) ( 1184 )   Save Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol (1 × 10-5 M) was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment.Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde. Related Articles | Metrics

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Silencing the gene encoding C/EBP homologous protein lessens acute brain injury following ischemia/reperfusion Fengzhang Wang, Yuan Zhang, Chunke He, Tingting Wang, Qiyan Piao, Qun Liu 2012, 7 (31):  2432-2438.  Abstract ( 208 )   PDF (257KB) ( 885 )   Save C/EBP homologous protein, an important transcription factor during endoplasmic reticulum stress,participates in cell apoptosis mediated by endoplasmic reticulum stress. Previous studies have shown that C/EBP homologous protein mediates nerve injury during Alzheimer’s disease,subarachnoid hemorrhage and spinal cord trauma. In this study, we introduced C/EBP homologous protein short hairpin RNA into the brains of ischemia/reperfusion rat models via injection of lentiviral vector through the left lateral ventricle. Silencing C/EBP homologous protein gene expression significantly reduced cerebral infarction volume, decreased water content and tumor necrosis factor-α and interleukin-1β mRNA expression in brain tissues following infarction, diminished the number of TUNEL-positive cells in the infarct region, decreased caspase-3 protein content and increased Bcl-2 protein content. These results suggest that silencing C/EBP homologous protein lessens cell apoptosis and inflammatory reactions, thereby protecting nerves. Related Articles | Metrics

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Arsenic exposure and glutamate-induced gliotransmitter release from astrocytes Yan Wang, Fenghong Zhao, Yingjun Liao, Yaping Jin, Guifan Sun 2012, 7 (31):  2439-2445.  Abstract ( 220 )   PDF (204KB) ( 1149 )   Save The present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 μM arsenite for 24 hours. Cell viability and morphological observations revealed that 5 μMarsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 μM arsenite for 24 hours and stimulated with 25 μM glutamate for 10 minutes. Results showed that [Ca2+]i in astrocytes exposed to 5 and 10 μM arsenite was significantly increased and levels of D-serine, γ-aminobutyric acid and glycine in cultures exposed to 2.5–10 μM arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 μM arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function. Related Articles | Metrics

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Therapeutic imaging window of cerebral infarction revealed by multisequence magnetic resonance imaging Hong Lu, Hui Hu, Zhanping He, Xiangjun Han, Jing Chen, Rong Tu 2012, 7 (31):  2446-2455.  Abstract ( 249 )   PDF (613KB) ( 811 )   Save In this study, we established a Wistar rat model of right middle cerebral artery occlusion and observed pathological imaging changes (T2-weighted imaging [T2WI], T2FLAIR, and diffusion-weighted imaging [DWI]) following cerebral infarction. The pathological changes were divided into three phases: early cerebral infarction, middle cerebral infarction, and late cerebral infarction. In the early cerebral infarction phase (less than 2 hours post-infarction), there was evidence of intracellular edema, which improved after reperfusion. This improvement was defined as the ischemic penumbra. In this phase, a high DWI signal and a low apparent diffusion coefficient were observed in the right basal ganglia region. By contrast, there were no abnormal T2WI and T2FLAIR signals. For the middle cerebral infarction phase (2–4 hours post-infarction), a mixed edema was observed. After reperfusion, there was a mild improvement in cell edema, while the angioedema became more serious. A high DWI signal and a low apparent diffusion coefficient signal were observed, and some rats showed high T2WI and T2FLAIR signals. For the late cerebral infarction phase (4–6 hours post-infarction), significant angioedema was visible in the infarction site.After reperfusion, there was a significant increase in angioedema, while there was evidence of hemorrhage and necrosis. A mixed signal was observed on DWI, while a high apparent diffusion coefficient signal, a high T2WI signal, and a high T2FLAIR signal were also observed. All 86 cerebral infarction patients were subjected to T2WI, T2FLAIR, and DWI. MRI results of clinic data similar to the early infarction phase of animal experiments were found in 51 patients, for which 10 patients (10/51) had an onset time greater than 6 hours. A total of 35 patients had MRI results similar to the middle and late infarction phase of animal experiments, of which eight patients (8/35) had an onset time less than 6 hours. These data suggest that defining the “therapeutic time window” as the time 6 hours after infarction may not be suitable for all patients. Integrated application of MRI sequences including T2WI, T2FLAIR, DW-MRI, and apparent diffusion coefficient mapping should be used to examine the ischemic penumbra, which may provide valuable information for identifying the “therapeutic time window”. Related Articles | Metrics

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Gait improvement after treadmill training in ischemic stroke survivors A critical review of functional MRI studies Xiang Xiao, Dongfeng Huang, Bryan O’Young 2012, 7 (31):  2457-2464.  Abstract ( 204 )   PDF (225KB) ( 991 )   Save Stroke survivors often present with abnormal gait, movement training can improve the walking performance post-stroke, and functional MRI can objectively evaluate the brain functions before and after movement training. This paper analyzes the functional MRI changes in patients with ischemic stroke after treadmill training with voluntary and passive ankle dorsiflexion. Functional MRI showed that there are some changes in some regions of patients with ischemic stroke including primary sensorimotor cortex, supplementary motor area and cingulate motor area after treadmill training.These findings suggest that treadmill training likely improves ischemic stroke patients’ lower limb functions and gait performance and promotes stroke recovery by changing patients’ brain plasticity;meanwhile, the novel treadmill training methods can better training effects. Related Articles | Metrics

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Repetitive transcranial magnetic stimulation improves consciousness disturbance in stroke patients A quantitative electroencephalography spectral power analysis Ying Xie, Tong Zhang 2012, 7 (31):  2465-2472.  Abstract ( 251 )   PDF (192KB) ( 868 )   Save Repetitive transcranial magnetic stimulation is a noninvasive treatment technique that can directly alter cortical excitability and improve cerebral functional activity in unconscious patients. To investigate the effects and the electrophysiological changes of repetitive transcranial magnetic stimulation cortical treatment, 10 stroke patients with non-severe brainstem lesions and with disturbance of consciousness were treated with repetitive transcranial magnetic stimulation. A quantitative electroencephalography spectral power analysis was also performed. The absolute power in the alpha band was increased immediately after the first repetitive transcranial magnetic stimulation treatment, and the energy was reduced in the delta band. The alpha band relative power values slightly decreased at 1 day post-treatment, then increased and reached a stable level at 2 weeks post-treatment. Glasgow Coma Score and JFK Coma Recovery Scale-Revised score were improved. Relative power value in the alpha band was positively related to Glasgow Coma Score and JFK Coma Recovery Scale-Revised score. These data suggest that repetitive transcranial magnetic stimulation is a noninvasive, safe, and effective treatment technology for improving brain functional activity and promoting awakening in unconscious stroke patients. Related Articles | Metrics

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Atypical clinical and pathological findings in a patient with isolated cortical vein thrombosis Yan Ding, Vance Fredrickson, Yicong Lin, Yueshan Piao, Xiangbo Wang, Dehong Lu,Cunjiang Li 2012, 7 (31):  2473-2479.  Abstract ( 200 )   PDF (229KB) ( 821 )   Save Isolated cortical vein thrombosis often produces a focal lesion. Because of the rapid development of collateral circulation, increased intracranial pressure has never been reported in a patient with isolated cortical vein thrombosis. The diagnosis of isolated cortical vein thrombosis is based mainly on MRI, catheter digital subtraction angiography, and histological findings, but may be challenging.We report a patient who presented with intermittent seizures and left-sided limb weakness. Her symptoms gradually progressed, and she eventually developed signs of increased intracranial pressure. Imaging studies showed a space-occupying lesion in the right frontal lobe of the brain. As we could not diagnose isolated cortical vein thrombosis based on the preoperative findings, surgical excision of the lesion was performed under general anesthesia. Histological examination showed destruction of the brain parenchyma with infiltration of macrophages, proliferation of reactive astrocytes and small vessels, and foci of hemorrhage. Further examination found that a number of small vessels in both the subarachnoid space and brain parenchyma were filled with thrombus,some of which was organized. Elastic fiber staining showed that the obstructed vessels were veins.We diagnosed isolated cortical vein thrombosis with atypical clinical features. Related Articles | Metrics