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Expression of mRnA-encoding subunits of n-methyl-d-aspartate receptor in the hypothalamus in sustained monaural block of auditory air-conduction model rats

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neural Regeneration Research 2011年第14期6卷 1062-1066页

作者： Ping Wan Xiaojian Lai Cheng Huang Xinde Sun department of Biology College of Life and Environmental Sciences Shanghai Normal University Shanghai 200234 China College of Physical and Health Education East China Normal University Shanghai 200062 China College of Chinese Medicine Shanghai University of Traditional Chinese Medicine Shanghai 201203 China department of Biology College of Life Sciences East China Normal University Shanghai 200062 China

A sustained monaural block of auditory air-conduction model was established in rats through subcutaneous suture in the right ear canal.The gene expression levels of hypothalamic n-methyl-d-aspartate receptor nR1,nR2A,nR2B and nR2C mRnA in the auditory central nervous system of Sprague-dawley rats at postnatal 9,23,37 days were determined after an environmental change.Reverse transcription-PCR assay showed that the critical period for the development of nR1,nR2A,and nR2B subunits in the left hypothalamus and nR1-and nR2B-dependent auditory neurons in the right hypothalamus terminated 23 days after the suture in the right ear.The critical period for the development of nR2A subunit-dependent auditory neurons in the right hypothalamus was terminated by postnatal day 37.The results confirmed that n-methyl-d-aspartate receptor subunits in the hypothalamus may be regulated by the auditory environment.

关键词： auditory air-conduction block N-methyI-D-aspartate receptor subunit hypothalamus gene expression neural regeneration

n-methyl-d-aspartate receptor subunit 1 protein expression in the hippocampus and temporal cortex of kainic acid-induced epilepsy rats

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neural Regeneration Research 2010年第14期5卷 1045-1049页

作者： Zan Wang Hongyu Jiang Suisheng Wu Hongmei Meng Li Ji Li Cui Weihong Lin department of neurology First Hospital of Jilin University Changchun 130021 Jilin Province China

BACKGROUnd： The n-methyl-d-aspartate receptor subunit 1 （nMdAR1） contributes to the incidence of epilepsy. However, the relationship between epilepsy-induced brain injury and nMdAR1 remains poorly understood. OBJECTIVE： To investigate changes in nMdAR1 protein expression in the hippocampus and temporal cortex of kainic acid-induced epilepsy rats. dESIGn, TIME And SETFInG： A randomized, controlled, animal experiment was performed at the department of Physiology and department of Pathology, Basic Medical College of Jilin University from March 2002 to March 2003. MATERIALS： Rabbit anti-nMdAR1 antibody was purchased from Wuhan Boster Biological Technology, China. METHOdS： A total of 80 healthy, male, Wistar rats, aged 22 weeks, were randomly assigned to sham-surgery （n = 10） and model （n = 70） groups. Epilepsy models were established by injecting kainic acid （1μL） into the right amygdala, and rats were sacrificed at 2, 6, 24, 72 hours, and 7, 15, 30 days after surgery, with 10 animals at each time point. The rats in the sham-surgery group were injected with 1μL phosphate buffered saline into the right amygdala. MAIn OUTCOME MEASURES： nMdAR1 protein expression in the hippocampus and temporal cortex at 2, 6, 24, 72 hours and 7, 15, 30 days after epilepsy was detected using immunohistochemistry and flow cytometry analysis. RESULTS： In the sham-surgery group, a few nMdARl-positive cells were distributed in the hippocampus and temporal cortex. In the model group, nMdARl-positive cells were increased in the hippocampus and temporal cortex at 2 hours following kainic acid-induced epilepsy. They were significantly increased at 6 hours, and slightly decreased at 7 days （CA3 region and temporal cortex）, but remained greater than the sham-surgery group. This continued until day 30 （P 〈 0.01 ）. In addition, there were more nMdAR1 positive cells in the hippocampal CA3 and dentate gyrus than the temporal cortex （P 〈 0.01）. COnCLUSIOn： In epilepsy model rats, nMdAR1 protein expression was upregulated in the hippocampus and

关键词： kainic acid epilepsy N-methyI-D-aspartate receptor rat subunit neural regeneration

Curcumin protects against ischemic spinal cord injury The pathway effect

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neural Regeneration Research 2013年第36期8卷 3391-3400页

作者： Jinhua Zhang Hao Wei Meimei Lin Chunmei Chen Chunhua Wang Maobai Liu department of Pharmacy Union Hospital Fujian Medical University department of neurosurgery Union Hospital Fujian Medical University

Inducible nitric oxide synthase and N-methyI-D-aspartate receptors have been shown to participate in nerve cell injury during spinal cord ischemia. This study observed a protective effect of curcumin on ischemic spinal cord injury. Models of spinal cord ischemia were established by ligating the lumbar artery from the left renal artery to the bifurcation of the abdominal aorta. At 24 hours after model establishment, the rats were intraperitoneally injected with curcumin, Reverse transcrip- tion-polymerase chain reaction and immunohistochemical results demonstrated that after spinal cord ischemia, inducible nitric oxide synthase and N-methyI-D-aspartate receptor mRnA and protein expression significantly increased. However, curcumin significantly decreased inducible nitric oxide synthase and N-methyI-D-aspartate receptor mRnA and protein expression in the ischemic spinal cord. Tadov scale results showed that curcumin significantly improved motor function of the rat hind limb after spinal cord ischemia. The results demonstrate that curcumin exerts a neuroprotective ef- fect against ischemic spinal cord injury by decreasing inducible nitric oxide synthase and N-methyI-D-aspartate receptor expression.

关键词： neural regeneration traditional Chinese medicine curcumin spinal cord injury ischemic injury N-methyI-D-aspartate receptor inducible nitric oxide synthase neuroprotection grants-supported paper neuroregeneration

Chronic pre-treatment with memantine prevents amyloid-beta protein-mediated long-term potentiation disruption

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neural Regeneration Research 2013年第1期8卷 49-55页

作者： Fushun Li Xiaowei Chen Feiming Wang Shujun Xu Lan Chang Roger Anwyl Qinwen Wang department of Physiology Medical School Research Center of Behavioral Science Ningbo University Zhenhai High School Trinity College Institute of neuroscience Department of Physiology Trinity College

Previous studies indicate that memantine, a low-affinity N-methyI-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.

关键词： neural regeneration neurodegenerative diseases memantine amyloid-β protein long-termpotentiation synaptic plasticity N-methyI-D-aspartate receptor Alzheimer＇s disease hippocampusgrants-supported paper neuroregeneration

neuroprotective effect of penehyclidine hydrochloride on focal cerebral ischemia-reperfusion injury

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neural Regeneration Research 2013年第7期8卷 622-632页

作者： Cuicui Yu Junke Wang department of Anesthesiology First Affiliated Hospital of China Medical University department of Anesthesiology Affiliated Yuhuangding Hospital Medical College of Qingdao University

Penehyclidine hydrochloride can promote microcirculation and reduce vascular permeability. However, the role of penehyclidine hydrochlodde in cerebral ischemia-reperfusion injury remains unclear. In this study, in vivo middle cerebral artery occlusion models were established in experimental rats, and penehyclidine hydrochloride pretreatment was given via intravenous injection prior to model establishment. Tetrazolium chloride, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling and immunohistochemical staining showed that, penehyclidine hydrochloride pretreatment markedly attenuated neuronal histopathological changes in the cortex, hippocampus and striatum, reduced infarction size, increased the expression level of BcI-2, decreased the expression level of caspase-3, and inhibited neuronal apoptosis in rats with cerebral ischemia-reperfusion injury. Xanthine oxidase and thiobarbituric acid chromogenic results showed that penehyclidine hydrochloride upregulated the activity of superoxide dismutase and downregulated the concentration of malondialdehyde in the ischemic cerebral cortex and hippocampus, as well as reduced the concentration of extracellular excitatory amino acids in rats with cerebral ischemia-reperfusion injury. In addition, penehyclidine hydrochloride inhibited the expression level of the nR1 subunit in hippocampal nerve cells in vitro following oxygen-glucose deprivation, as detected by PCR. Experimental findings indicate that penehyclidine hydrochloride attenuates neuronal apoptosis and oxidative stress injury after focal cerebral ischemia-reperfusion, thus exerting a neuroprotective effect.

关键词： neural regeneration brain injury penehyclidine hydrochloride cerebral ischemia-reperfusion injuryischemic cerebrovascular disease apoptosis excitatory amino acid oxygen free radicals superoxide dismutase N-methyI-D-aspartate receptor middle cerebral artery occlusion oxygen-glucose deprivation photographs-containing paper neuroregeneration

Anti-epileptic effects of neuropeptide Y gene transfection into the rat brain

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neural Regeneration Research 2013年第14期8卷 1307-1315页

作者： Changzheng dong Wenqing Zhao Wenling Li Peiyuan Lv Xiufang dong Faculty of Graduate Studies Hebei Medical University department of Functional neurosurgery Hebei General Hospital department of neurology Hebei General Hospital department of neurology First Hospital of Xingtai

neuropeptide Y gene transfection into normal rat brain tissue can provide gene overexpression, which can attenuate the severity of kainic acid-induced seizures. In this study, a recombinant adeno-associated virus carrying the neuropeptide Y gene was transfected into brain tissue of rats with kainic acid-induced epilepsy through stereotactic methods. Following these transfections, we verified overexpression of the neuropeptide Y gene in the epileptic brain. Electroencephalograms showed that seizure severity was significantly inhibited and seizure latency was significantly prolonged up to 4 weeks after gene transfection. Moreover, quantitative fluorescent PCR and western blot assays revealed that the mRnA and protein expression of the N-methyI-D-aspartate receptor subunits nR1, nR2A, and nR2B was inhibited in the hippocampus of epileptic rats. These findings indicate that neuropeptide Y may inhibit seizures via down-regulation of the functional expression of N-methyI-D-aspartate receptors.

关键词： neural regeneration brain injury gene therapy adeno-associated virus neuropeptide Y epilepsy N-methyI-D-aspartate receptor kainic acid seizures neuroregeneration

Glycolysis in energy metabolism during seizures

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neural Regeneration Research 2013年第14期8卷 1316-1326页

作者： Heng Yang Jiongxing Wu Ren Guo Yufen Peng Wen Zheng ding Liu Zhi Song department of neurology Third Xiangya HospitalCentral South University department of Pharmacy Third Xiangya HospitalCentral South University

Studies have shown that glycolysis increases during seizures, and that the glycolytic metabolite lactic acid can be used as an energy source. However, how lactic acid provides energy for seizures and how it can participate in the termination of seizures remains unclear. We reviewed possible mechanisms of glycolysis involved in seizure onset. Results showed that lactic acid was involved in seizure onset and provided energy at early stages. As seizures progress, lactic acid reduces the pH of tissue and induces metabolic acidosis, which terminates the seizure. The specific mechanism of lactic acid-induced acidosis involves several aspects, which include lactic acid-induced inhibition of the glycolytic enzyme 6-diphosphate kinase-1, inhibition of the n-methyl-d-aspartate receptor, activation of the acid-sensitive 1A ion channel, strengthening of the receptive mechanism of the inhibitory neurotransmitter Y-aminobutyric acid, and changes in the intra- and extracellular environment.

关键词： neural regeneration reviews epilepsy energy metabolism glycolysis epileptogenesis terminationATP aerobic metabolism 6-diphosphate kinase-1 N-methyI-D-aspartate receptor acid-sensitive1A ion channel y-aminobutyric acid intra- and extracellular environment voltage-gated na＋ andCa2＋ adenosine receptors ATP receptor grants-supported paper neuroregeneration

differentiation renders susceptibility to excitotoxicity in HT22 neurons

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neural Regeneration Research 2013年第14期8卷 1297-1306页

作者： Minchao He Jun Liu haowu Cheng Yigang Xing William Z Suo department of neurology Sun Yat-sen Memorial HospitalSun Yat-sen University Laboratory for Alzheimer's disease & Aging Research Veterans Affairs Medical Center department of neurology University of Kansas Medical Center Molecular & Integrative Physiology University of Kansas Medical Center

HT22 is an immortalized mouse hippocampal neuronal cell line that does not express cholinergic and glutamate receptors like mature hippocampal neurons in vivo. This in part prevents its use as a model for mature hippocampal neurons in memory-related studies. We now report that HT22 cells were appropriately induced to differentiate and possess properties similar to those of mature hippocampal neurons in vivo, such as becoming more glutamate-receptive and excitatory. Results showed that sensitivity of HT22 cells to glutamate-induced toxicity changed dramatically when comparing undifferentiated with differentiated cells, with the half-effective concentration for differentiated cells reducing approximately two orders of magnitude. Moreover, glutamate-induced toxicity in differentiated cells, but not undifferentiated cells, was inhibited by the n-methyi-d- aspartate receptor antagonists MK-801 and memantine. Evidently, differentiated HT22 cells expressed N-methyI-D-aspartate receptors, while undifferentiated cells did not. Our experimental findings indicated that differentiation is important for immortalized cell lines to render post-mitotic neuronal properties, and that differentiated HT22 neurons represent a better model of hippocampal neurons than undifferentiated cells.

关键词： neural regeneration brain injury HT22 differentiation N-methyI-D-aspartate receptor glutamateexcitatory neurotoxicity mitosis hippocampus neurons MK-801＂ memantine grants-supportedpaper neuroregeneration

Protective effect of oxysophoridine on cerebral ischemia/reperfusion injury in mice

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neural Regeneration Research 2013年第15期8卷 1349-1359页

作者： Hongbo Wang Yuxiang Li ning Jiang Xiaoping Chen Yi Zhang Kuai Zhang Tengfei Wang Yinju Hao Lin Ma Chengjun Zhao Yanrong Wang Tao Sun Jianqiang Yu department of Pharmacology Ningxia Medical University College of nursing Ningxia Medical University Shanghai Pudong new Area Gongli Hospital ningxia Key Laboratory of Craniocerebral diseases of ningxia Hui Autonomous Region School of Basic Medical Sciences Ningxia Medical University Key Laboratory of Reproduction and Genetics of ningxia Medical University Collaborative Innovation Center of ningxia Hui Autonomous Region for Medicines

Oxysophoridine, a new alkaloid extracted from Sophora alopecuroides L., has been shown to have a protective effect against ischemic brain damage. In this study, a focal cerebral ischemia/reperfusion injury model was established using middle cerebral artery occlusion in mice. Both 62.5, 125, and 250 mg/kg oxysophoridine, via intraperitoneal injection, and 6 mg/kg nimodipine, via intragastric administration, were administered daily for 7 days before modeling. After 24 hours of reperfusion, mice were tested for neurological deficit, cerebral infarct size was assessed and brain tissue was collected. Results showed that oxysophoridine at 125, 250 mg/kg and 6 mg/kg nimodipine could reduce neurological deficit scores, cerebral infarct size and brain water content in mice. These results provided evidence that oxysophoridine plays a protective role in cerebral ischemia/reperfusion injury. In addition, oxysophoridine at 62.5, 125, and 250 mg/kg and 6 mg/kg nimodipine increased adenosine-triphosphate content, and decreased malondialdehyde and nitric oxide content. These compounds enhanced the activities of glutathione-peroxidase, superoxide dismutase, catalase, and lactate dehydrogenase, and decreased the activity of nitric oxide synthase Protein and mRnA expression levels of N-methyI-D-aspartate receptor subunit nR1 were markedly inhibited in the presence of 250 mg/kg oxysophoridine and 6 mg/kg nimodipine. Our experimental findings indicated that oxysophoridine has a neuroprotective effect against cerebral ischemia/reperfusion injury in mice, and that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyI-D-aspartate receptor subunit nR1.

关键词： neural regeneration traditional Chinese medicine brain injury oxysophoridine ischemia/reperfusion injury oxidative stress N-methyI-D-aspartate receptor neuroprotection grants-supported paper neuroregeneration