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中国临床康复 2005年第1期9卷 146-148页

作者：王国卿封丽芳夏作理泰山医学院脑微循环研究所山东省泰安市271000 博兴中医医院山东省博兴市256500

目的:综述星形胶质细胞活化的机制及功能变化特点,为通过活化星形胶质细胞的功能变化来改善神经元修复提供有益的提示。资料来源:用计算机检索Medline,Pubmed,Springer和PML数据库1995-01/2004-04与星形胶质细胞的生物学功能与神经元修... 详细信息

目的:综述星形胶质细胞活化的机制及功能变化特点,为通过活化星形胶质细胞的功能变化来改善神经元修复提供有益的提示。资料来源:用计算机检索Medline,Pubmed,Springer和PML数据库1995-01/2004-04与星形胶质细胞的生物学功能与神经元修复相关的文章,检索词“astrocytefunction/acting,neuronrehabilitation/plerosis,并限定文章语言种类为English。同时计算机检索“中国全文期刊数据库”1995-01/2004-04与星形胶质细胞活化的机制及功能变化特点相关的文章,限定文章语言种类为中文,检索词星形胶质细胞生物学“功能/活化,神经元发育/营养/修复/损伤。资料选择:对资料进行初审,纳入标准:选择与星形胶质细胞生物学功“能、活化,神经元发育、营养、修复及损伤”有关文章,在1995年以后发表的文章。排除标准:综述类文章,重复文章。资料提炼:共搜集到201篇相关文章,入选17篇,因为这些文章能包含其他文章的内容,且发表时间为1996/2004期间。资料综合:对检索到的文章的相关信息综合加以概括综述,其中星形胶质细胞生物学功能、活化13篇,星形胶质细胞生物学功能与神经元损伤修复的17篇。结论:星形胶质细胞生物学功能复杂,多途径影响神经元的修复;但对神经元的影响有双重性。

关键词：神经元星形细胞/生理学综述文献

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星形胶质细胞对神经元作用的研究进展

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浙江大学学报（医学版） 2008年第5期37卷 531-536页

作者：王建彪(综述) 竺可青(综述) 浙江大学医学院病理学与法医学研究所神经科学研究所浙江杭州310058

星形胶质细胞能够释放多种胶质细胞源性递质,调节突触信号的传递;释放的雌激素、凝血栓蛋白、IL-1β和IL-6能够诱导突触的形成和神经干细胞的神经发生。此外,星形胶质细胞还能为神经元提供重要的营养和保护作用。星形胶质细胞可能是治... 详细信息

星形胶质细胞能够释放多种胶质细胞源性递质,调节突触信号的传递;释放的雌激素、凝血栓蛋白、IL-1β和IL-6能够诱导突触的形成和神经干细胞的神经发生。此外,星形胶质细胞还能为神经元提供重要的营养和保护作用。星形胶质细胞可能是治疗某些神经系统疾病的新靶点。

关键词：星形细胞/生理学神经元/生理学中枢神经系统/生理学

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Evidence for chloride ions as intracellular messenger substances in astrocytes

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JOURNAL OF NEUROPHYSIOLOGY 1999年第1期82卷 248-254页

作者： Bekar, LK Walz, W Univ Saskatchewan Dept Physiol Saskatoon SK S7N 5E5 Canada

Evidence for chloride ions as intracellular messenger substances in astrocytes. J. Neurophysiol:. 82. 248-254, 1999. Cultured rat hippocampal astrocytes were used to investigate the mechanism underlying the suppression of Ba2+-sensitive K+ currents by GABA, receptor activation. Muscimol application had two effects on whole cell currents: opening of the well-known Cl- channel of the GABA, receptor and a secondary longerlasting blockade of outward K+ currents displaying both peak and plateau phases. This blockade was independent of both Na+ (inside and outside) and ATP in the pipette. It also seemed to be independent of muscimol binding to the receptor because picrotoxin application showed no effect on the K+ conductance. The effect is blocked when anion efflux is prevented by replacing Cl- with gluconate (both inside and out) and is enhanced with more permeant anions such as Br- and I-. Moreover, the effect is reproduced in the absence of muscimol by promoting Cl- efflux via lowering of extracellular Cl- levels. These results, along with the requirement for Cl- efflux in muscimol experiments, show a strong dependency of the secondary blockade on Cl- efflux through the Cl- channel of the GABA, receptor. We therefore conclude that changes in the intracellular Cl- concentration alter the outward K+ conductances of astrocytes. Such a Cl--mediated modulation of an astrocytic K+ conductance will have important consequences for the progression of spreading depression through brain tissue and for astrocytic swelling in pathological situations.

关键词：动物新生星形细胞/细胞学星形细胞/药物作用星形细胞/生理学钡/药理学细胞培养的氯化物通道/生理学氯化物/生理学葡糖酸盐类/药理学海马/生理学动力学蝇蕈醇/药理学钾通道/药物作用钾通道/生理学大鼠 Wistar 受体 GABA-A/生理学第二信使系统钠/药理学钠/生理学动物大鼠

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Expression of CX₃CR1 chemokine receptors on neurons and their role in neuronal survival

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第14期97卷 8075-8080页

作者： Meucci, O Fatatis, A Simen, AA Miller, RJ Univ Chicago Dept Neurobiol Pharmacol & Physiol Chicago IL 60637 USA Univ Chicago Comm Neurobiol Chicago IL 60637 USA

Recent in vitro and in vivo studies have shown that the chemokine fractalkine is widely expressed in the brain and localized principally to neurons. Central nervous system expression of CX(3)CR1, the only known receptor for fractalkine, has been demonstrated exclusively on microglia and astrocytes. Thus, it has been proposed that fractalkine regulates cellular communication between neurons (that produce fractalkine) and microglia (that express its receptor). Here we show, for the first time, that hippocampal neurons also express CX(3)CR1. Receptor activation by soluble fractalkine induces activation of the protein kinase Akt, a major component of prosurvival signaling pathways, and nuclear translocation of NF-KB, a downstream effector of Akt. Fractalkine protects hippocampal neurons from the neurotoxicity induced by the HIV-1 envelope protein gp120(IIIB), an effect blocked by anti-CX(3)CR1 antibodies, Experiments with two different inhibitors of the phosphatidylinositol 3-kinase, a key enzyme in the activation of Akt, and with a phospholipid activator of Akt demonstrate that Akt activation is responsible for the neuroprotective effects of fractalkine. These data show that neuronal CX(3)CR1 receptors mediate the neurotrophic effects of fractalkine, suggesting that fractalkine and its receptor are involved in a complex network of both paracrine and autocrine interactions between neurons and glia.

关键词：星形细胞/生理学细胞存活趋化因子CX3CL1 趋化因子 CX3C 趋化因子 CXC/代谢培养技术/方法 DNA结合蛋白质类/代谢海马/细胞学 I-κB蛋白质类膜蛋白质类/代谢 NF-κB/代谢神经元/生理学磷脂酰肌醇类/代谢蛋白质丝氨酸苏氨酸激酶原癌基因蛋白质类/代谢原癌基因蛋白质c-akt 受体细胞因子/遗传学受体细胞因子/代谢受体 HIV/遗传学受体 HIV/代谢重组蛋白质类/代谢信号传导动物大鼠

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Astrocyte-mediated potentiation of inhibitory synaptic transmission

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NATURE NEUROSCIENCE 1998年第8期1卷 683-692页

作者： Kang, J Jiang, L Goldman, SA Nedergaard, M New York Med Coll Dept Cell Biol & Anat Valhalla NY 10595 USA Cornell Univ Coll Med Dept Neurol & Neurosci New York NY 10021 USA

We investigated the role of astrocytes in activity-dependent modulation of inhibitory synaptic transmission in hippocampal slices. Repetitive firing of an interneuron decreased the probability of synaptic failures in spike-evoked inhibitory postsynaptic currents (unitary IPSCs) in CA1 pyramidal neurons. The GABA(B)-receptor antagonist CCP55845A abolished this effect. Direct stimulation of astrocytes, or application of the GABA(B)-receptor agonist baclofen, potentiated miniature inhibitory postsynaptic currents (mIPSCs) in pyramidal neurons. These effects were blocked by inhibition of astrocytic calcium signaling with the calcium chelator BAPTA or by antagonists of the ionotropic glutamate receptors. These observations suggest that interneuronal firing elicits a GABA(B)-receptor-mediated elevation of calcium in surrounding astrocytes, which in turn potentiates inhibitory transmission. Astrocytes may therefore be a necessary intermediary in activity-dependent modulation of inhibitory synapses in the hippocampus.

关键词：星形细胞/生理学钙信号/生理学海马/细胞学海马/生理学神经抑制/生理学神经胶质/生理学神经元/生理学大鼠 Sprague-Dawley 受体 AMPA/生理学受体 N-甲基-D-天冬氨酸/生理学突触/生理学突触传递/生理学动物女(雌)性男(雄)性大鼠

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Potent blockade of sodium channels and protection of brain tissue from ischemia by BIII890CL

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第9期97卷 4944-4949页

作者： Carter, AJ Grauert, M Pschorn, U Bechtel, WD Bartmann-Lindholm, C Qu, YS Scheuer, T Catterell, WA Weiser, T Boehringer Ingelheim Pharma KG Dept Cent Nervous Syst Res D-55216 Ingelheim Germany Boehringer Ingelheim Pharma KG Dept Med Chem D-55216 Ingelheim Germany Univ Washington Dept Pharmacol Seattle WA 98195 USA

We have synthesized a new benzomorphan derivative, 2R-[2 alpha,3(S*),6 alpha]-1,2,3,4,5,6-hexahydro-6,11,11-trimethyl-3-[2-(phenylmethoxy)propyl]-2,6-methano-3-benzazocin-10-ol hydrochloride (BIII 890 CL), which displaced [H-3]batrachotoxinin A-20 alpha-benzoate from neurotoxin receptor site 2 of the Na+ channel in rat brain synaptosomes (IC50 = 49 nM), but exhibited only low affinity for 65 other receptors and ion channels. BIII 890 CL inhibited Na+ channels in cells transfected with type IIA Na+ channel or subunits and shifted steady-state inactivation curves to more negative potentials. The IC50 value for the inactivated Na+ channel was much lower (77 nM) than for Na+ channels in the resting state (18 mu M) Point mutations F1764A and Y1771A in transmembrane segment S6 in domain IV of the alpha subunit reduced the voltage- and frequency-dependent block, findings which suggest that BIII 890 CL binds to the local anesthetic receptor site in the pore, BIII 890 CL inhibited veratridine-induced glutamate release in brain slices, as well as glutamate release and neurotoxicity in cultured cortical neurons. BIII 890 CL (3-30 mg/kg s,c.) reduced lesion size in mice and rats when administered 5 min after permanent focal cerebral ischemia at doses that did not impair motor coordination. In contrast to many other agents, BIII 890 CL was neuroprotective in both cortical and subcortical regions of the rat brain. Our results demonstrate that BIII 890 CL is a potent, selective, and highly use-dependent Na+ channel blocker that protects brain tissue from the deleterious effects of focal cerebral ischemia in rodents.

关键词：动物新生星形细胞/药物作用星形细胞/生理学苯吗吩烷类/药理学结合竞争性脑/生理学细胞培养的大脑皮质/药物作用大脑皮质/生理学纹状体/药物作用纹状体/生理学谷氨酸/代谢脑缺血发作短暂性/病理生理学脑缺血发作短暂性/预防和控制膜电位/药物作用膜电位/生理学小鼠近交系运动活动/药物作用神经保护药/药理学大鼠 Wistar 重组蛋白质类/代谢钠通道阻滞剂钠通道/化学钠通道/生理学突触体/生理学转染藜芦定/药理学动物男(雄)性小鼠大鼠

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Meningeal cells can communicate with astrocytes by calcium signaling

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ANNALS OF NEUROLOGY 2000年第1期47卷 18-25页

作者： Grafstein, B Liu, SJ Cotrina, ML Goldman, SA Nedergaard, M Cornell Univ Weill Med Coll Dept Physiol & Biophys New York NY 10021 USA New York Med Coll Dept Cell Biol & Anat Valhalla NY 10595 USA

Mechanical stimulation of adult human and rat pia-arachnoid cell cultures (loaded with calcium indicator dye) produced an increase in calcium in the stimulated cell. This change then propagated rapidly among neighboring cells, producing a calcium wave with a maximum distance of propagation and velocity resembling calcium waves in astrocytes. The pia-arachnoid waves were blocked by either octanol or apyrase, suggesting that propagation might occur either by gap junction communication or extracellular movement of ATP. Calcium waves in pia-arachnoid cells could invade contiguous astrocytes, and vice versa. Gap junction coupling between pia-arachnoid cells and astrocytes was shown by dye transfer experiments, in conjunction with immunostaining for connexin43, We infer that calcium signals from cells in the cortical parenchyma may be transmitted to the pia-arachnoid and might then serve in the induction of neurovascular changes, including those postulated to be responsible for the pain of migraine headache.

关键词：星形细胞/细胞学星形细胞/生理学钙/代谢钙信号/生理学细胞间通讯/生理学细胞培养的脑膜/细胞学脑膜/生理学人类

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Interaction between astrocytes and adult subventricular zone precursors stimulates neurogenesis

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第13期96卷 7526-7531页

作者： Lim, DA Alvarez-Buylla, A Rockefeller Univ New York NY 10021 USA

Neurogenesis continues in the mammalian subventricular zone (SVZ) throughout life. However, the signaling and cell-cell interactions required for adult SVZ neurogenesis are not known. In vivo, migratory neuroblasts (type A cells) and putative precursors (type C cells) are in intimate contact with astrocytes (type B cells). Type B cells also contact each other. We reconstituted SVZ cell-cell interactions in a culture system free of serum or exogenous growth factors, Culturing dissociated postnatal or adult SVZ cells on astrocyte monolayers-but not other substrates-supported extensive neurogenesis similar to that observed in vivo. SVZ precursors proliferated rapidly on astrocytes to form colonies containing up to 100 type A neuroblasts. By fractionating the SVZ cell dissociates with differential adhesion to immobilized polylysine, we show that neuronal colony-forming precursors were concentrated in a fraction enriched for type B and C cells. Pure type A cells could migrate in chains but did not give rise to neuronal colonies. Because astrocyte-conditioned medium alone was not sufficient to support SVZ neurogenesis, direct cell-cell contact between astrocytes and SVZ neuronal precursors may be necessary for the production of type A cells.

关键词：星形细胞/细胞学星形细胞/生理学细胞间通讯/生理学细胞分化/生理学细胞运动/生理学细胞培养的神经元/细胞学神经元/生理学前脑/细胞学前脑/生理学成年人人类

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The optic nerve head in glaucoma: Role of astrocytes in tissue remodeling

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PROGRESS IN RETINAL AND EYE RESEARCH 2000年第3期19卷 297-321页

作者： Hernandez, MR Washington Univ Sch Med Dept Ophthalmol & Visual Sci St Louis MO 63110 USA Washington Univ Sch Med Dept Anat & Neurobiol St Louis MO 63110 USA

Primary open angle glaucoma is a common eye disease characterized by loss of the axons of the retinal ganglion cells leading to progressive loss of vision. The site of damage to the axons is at the level of the lamina cribrosa in the optic nerve head. The mechanism of axonal loss is unknown but elevated intraocular pressure and age are the most common factors associated with the disease. Previous studies in human glaucoma and in experimental glaucoma in monkeys have established a relationship between chronic elevation of intraocular pressure and remodeling of the optic nerve head tissues known clinically as cupping of the optic disc. This review focuses on the astrocytes, the major cell type in the optic nerve head. Astrocytes participate actively in the remodeling of neural tissues during development and in disease. In glaucomatous optic neuropathy, astrocytes play a major role in the remodeling of the extracellular matrix of the optic nerve head, synthesize growth factors and other cellular mediators that may affect directly, or indirectly, the axons of the retinal ganglion cells. Due to the architecture of the lamina cribrosa, formed by the cells and the fibroelastic extracellular matrix, astrocytes may respond to changes in intraocular pressure in glaucoma, leading to some of the detrimental events that underlie axonal loss and retinal ganglion cell degeneration. (C) 2000 Elsevier Science Ltd. All rights reserved.

关键词：星形细胞/生理学细胞外基质/生理学青光眼开角型/病理生理学生长物质/代谢整合素类/代谢神经生长因子类/代谢神经细胞黏附分子类/代谢视盘/病理生理学视网膜神经节细胞/生理学动物人类

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Inhibition of calcium/calmodulin kinase II alpha subunit expression results in epileptiform activity in cultured hippocampal neurons

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第10期97卷 5604-5609页

作者： Churn, SB Sombati, S Jakoi, ER Sievert, L DeLorenzo, RJ Virginia Commonwealth Univ Med Coll Virginia Dept Neurol Richmond VA 23298 USA Virginia Commonwealth Univ Med Coll Virginia Dept Anat & Neurosci Richmond VA 23298 USA Virginia Commonwealth Univ Med Coll Virginia Dept Pharmacol & Toxicol Richmond VA 23298 USA Virginia Commonwealth Univ Med Coll Virginia Dept Biochem & Biophys Richmond VA 23298 USA

Several models that develop epileptiform discharges and epilepsy have been associated with a decrease in the activity of calmodulin-dependent kinase II. However, none of these studies has demonstrated a causal relationship between a decrease in calcium/calmodulin kinase II activity and the development of seizure activity. The present study was conducted to determine the effect of directly reducing calcium/calmodulin-dependent kinase activity on the development of epileptiform discharges in hippocampal neurons in culture. Complimentary oligonucleotides specific for the alpha subunit of the calciumlcalmodulin kinase were used to decrease the expression of the enzyme. Reduction in kinase expression was confirmed by Western analysis, immunocytochemistry, and exogenous substrate phosphorylation. Increased neuronal excitability and frank epileptiform discharges were observed after a significant reduction in calmodulin kinase II expression. The epileptiform activity was a synchronous event and was not caused by random neuronal firing. Furthermore, the magnitude of decreased kinase expression correlated with the increased neuronal excitability. The data suggest that decreased calmodulin kinase II activity may play a role in epileptogenesis and the long-term plasticity changes associated with the development of pathological seizure activity and epilepsy.

关键词：动物新生星形细胞/细胞学星形细胞/生理学细胞分裂/药物作用细胞培养的阿糖胞苷/药理学癫痫/酶学癫痫/病理生理学基因表达调控酶学/药物作用海马/生理学突变误义神经胶质/细胞学神经胶质/药物作用神经元/细胞学神经元/酶学神经元/生理学寡脱氧核糖核苷酸类反义/药理学磷酰化动物大鼠

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