Neuron glia biology最新文献_第7页

Reactive astrocytosis and glial glutamate transporter clustering are early changes in a spinocerebellar ataxia type 1 transgenic mouse model. 反应性星形细胞增生和胶质谷氨酸转运蛋白聚集是1型脊髓小脑性共济失调转基因小鼠模型的早期变化。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000185

Roberto Giovannoni, Nicola Maggio, Maria Rosaria Bianco, Carlo Cavaliere, Giovanni Cirillo, Marialuisa Lavitrano, Michele Papa

{"title":"Reactive astrocytosis and glial glutamate transporter clustering are early changes in a spinocerebellar ataxia type 1 transgenic mouse model.","authors":"Roberto Giovannoni, Nicola Maggio, Maria Rosaria Bianco, Carlo Cavaliere, Giovanni Cirillo, Marialuisa Lavitrano, Michele Papa","doi":"10.1017/S1740925X08000185","DOIUrl":"https://doi.org/10.1017/S1740925X08000185","url":null,"abstract":"Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder caused by an expanded CAG trinucleotide repeats within the coding sequence of the ataxin-1 protein. In the present study, we used a conditional transgenic mouse model of SCA1 to investigate very early molecular and morphological changes related to the behavioral phenotype. In mice with neural deficits detected by rotarod performance, and simultaneous spatial impairments in exploratory activity and uncoordinated gait, we observed both significant altered expression and patchy distribution of excitatory amino acids transporter 1. The molecular changes observed in astroglial compartments correlate with changes in synapse morphology; synapses have a dramatic reduction of the synaptic area external to the postsynaptic density. By contrast, Purkinje cells demonstrate preserved structure. In addition, severe reactive astrocytosis matches changes in the glial glutamate transporter and synapse morphology. We propose these morpho-molecular changes are the cause of altered synaptic transmission, which, in turn, determines the onset of the neurological symptoms by altering the synaptic transmission in the cerebellar cortex of transgenic animals. This model might be suitable for testing drugs that target activated glial cells in order to reduce CNS inflammation.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"335-51"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X08000185","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27541168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 27

Transcriptional regulation of PSA-NCAM mediated neuron-glial plasticity in the adult hypothalamus. 成人下丘脑中PSA-NCAM介导的神经元-胶质可塑性的转录调控。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X07000701

Jyoti Parkash, Gurcharan Kaur

{"title":"Transcriptional regulation of PSA-NCAM mediated neuron-glial plasticity in the adult hypothalamus.","authors":"Jyoti Parkash, Gurcharan Kaur","doi":"10.1017/S1740925X07000701","DOIUrl":"https://doi.org/10.1017/S1740925X07000701","url":null,"abstract":"Gonadotropin releasing hormone (GnRH)-secreting neurons in mammal's project principally to the median eminence-arcuate (ME-ARC) region where they make contact with basal lamina and open into the pericapillary space of the primary hypophyseal portal plexus. In the present study we report the expression of polysialylated form of neural cell adhesion molecule (PSA-NCAM) on the cell bodies of GnRH-secreting neurons and on glial cells in the medial preoptic area (mPOA) of the hypothalamus in both the proestrous and diestrous phases of cycling rats, using dual immunohistofluorescent staining. Regulation of PSA-NCAM occurs via regulation of PSA biosynthesis by the polysialyltransferase enzyme (PST-1). Therefore, we studied the expression of PST mRNA and GnRH in GnRH-releasing cell bodies by combining fluorescent in situ hybridization with immunohistofluorescence, and expression of PST mRNA in the mPOA using northern blotting. We observed dynamic upregulation of PSA-NCAM on GnRH cell bodies in the proestrous phase, accompanied by enhanced expression of PST-1 mRNA. The present results indicate that PSA-NCAM has a permissive role in the structural remodeling of GnRH neurons. Enhanced expression of mRNA encoding PST-1 in the proestrous phase indicates that the biosynthesis of PSA and, thus, PSA-NCAM is regulated at the transcriptional level.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"299-307"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X07000701","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27543405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Adenosine dysfunction in astrogliosis: cause for seizure generation? 星形胶质细胞病的腺苷功能障碍：癫痫发作的原因？

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X0800015X

Tianfu Li, Jing Quan Lan, Bertil B Fredholm, Roger P Simon, Detlev Boison

{"title":"Adenosine dysfunction in astrogliosis: cause for seizure generation?","authors":"Tianfu Li, Jing Quan Lan, Bertil B Fredholm, Roger P Simon, Detlev Boison","doi":"10.1017/S1740925X0800015X","DOIUrl":"10.1017/S1740925X0800015X","url":null,"abstract":"Epilepsy is characterized by both neuronal and astroglial dysfunction. The endogenous anticonvulsant adenosine, the level of which is largely controlled by astrocytes, might provide a crucial link between astrocyte and neuron dysfunction in epilepsy. Here we have studied astrogliosis, a hallmark of the epileptic brain, adenosine dysfunction and the emergence of spontaneous seizures in a comprehensive approach that includes a new mouse model of focal epileptogenesis, mutant mice with altered brain levels of adenosine, and mice lacking adenosine A1 receptors. In wild-type mice, following a focal epileptogenesis-precipitating injury, astrogliosis, upregulation of the adenosine-removing astrocytic enzyme adenosine kinase (ADK), and spontaneous seizures coincide in a spatio-temporally restricted manner. Importantly, these spontaneous seizures are mimicked by untreated transgenic mice that either overexpress ADK in brain or lack A1 receptors. Conversely, mice with reduced ADK in the forebrain do not develop either astrogliosis or spontaneous seizures. Our studies define ADK as a crucial upstream regulator of A1 receptor-mediated modulation of neuronal excitability, and support the ADK hypothesis of epileptogenesis in which upregulation of ADK during astrogliosis provides a crucial link between astrocyte and neuron dysfunction in epilepsy. These findings define ADK as rational target for therapeutic intervention.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"353-66"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561997/pdf/nihms51207.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27541169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acetylcholine inhibits cell cycle progression in rat Schwann cells by activation of the M2 receptor subtype. 乙酰胆碱通过激活M2受体亚型抑制大鼠雪旺细胞的细胞周期进程。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000045

Simona Loreti, Ruggero Ricordy, M Egle De Stefano, Gabriella Augusti-Tocco, Ada Maria Tata

{"title":"Acetylcholine inhibits cell cycle progression in rat Schwann cells by activation of the M2 receptor subtype.","authors":"Simona Loreti, Ruggero Ricordy, M Egle De Stefano, Gabriella Augusti-Tocco, Ada Maria Tata","doi":"10.1017/S1740925X08000045","DOIUrl":"https://doi.org/10.1017/S1740925X08000045","url":null,"abstract":"Cultures of Schwann cells from neonatal rat sciatic nerves were treated with acetylcholine agonists and the effects on cell proliferation evaluated. (3)[H]-thymidine incorporation shows that acetylcholine (ACh) receptor agonists inhibit cell proliferation, and FACS analysis demonstrates cell-cycle arrest and accumulation of cells in the G1 phase. The use of arecaidine, a selective agonist of muscarinic M2 receptors reveals that this effect depends mainly on M2 receptor activation. The arecaidine dependent-block in G1 is reversible because removal of arecaidine from the culture medium induces progression to the S phase. The block of the G1-S transition is also characterized by modulation of the expression of several cell-cycle markers. Moreover, treatment with ACh receptor agonist causes both a decrease in the PCNA protein levels in Schwann cell nuclei and an increase in p27 and p53 proteins. Finally, immuno-electron microscopy demonstrates that M2 receptors are expressed by Schwann cells in vivo. These results indicate that ACh, by modulating Schwann cell proliferation through M2 receptor activation, might contribute to their progression to a more differentiated phenotype.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"269-79"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X08000045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27543402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 41

Neuronal-glial interactions in central nervous system neurogenesis: the neural stem cell perspective. 中枢神经系统神经发生中的神经元-胶质相互作用：神经干细胞的观点。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X0800001X

Angela Gritti, Luca Bonfanti

{"title":"Neuronal-glial interactions in central nervous system neurogenesis: the neural stem cell perspective.","authors":"Angela Gritti, Luca Bonfanti","doi":"10.1017/S1740925X0800001X","DOIUrl":"10.1017/S1740925X0800001X","url":null,"abstract":"Essentially, three neuroectodermal-derived cell types make up the complex architecture of the adult CNS: neurons, astrocytes and oligodendrocytes. These elements are endowed with remarkable morphological, molecular and functional heterogeneity that reaches its maximal expression during development when stem/progenitor cells undergo progressive changes that drive them to a fully differentiated state. During this period the transient expression of molecular markers hampers precise identification of cell categories, even in neuronal and glial domains. These issues of developmental biology are recapitulated partially during the neurogenic processes that persist in discrete regions of the adult brain. The recent hypothesis that adult neural stem cells (NSCs) show a glial identity and derive directly from radial glia raises questions concerning the neuronal-glial relationships during pre- and post-natal brain development. The fact that NSCs isolated in vitro differentiate mainly into astrocytes, whereas in vivo they produce mainly neurons highlights the importance of epigenetic signals in the neurogenic niches, where glial cells and neurons exert mutual influences. Unravelling the mechanisms that underlie NSC plasticity in vivo and in vitro is crucial to understanding adult neurogenesis and exploiting this physiological process for brain repair. In this review we address the issues of neuronal/glial cell identity and neuronal-glial interactions in the context of NSC biology and NSC-driven neurogenesis during development and adulthood in vivo, focusing mainly on the CNS. We also discuss the peculiarities of neuronal-glial relationships for NSCs and their progeny in the context of in vitro systems.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"309-23"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27541166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adhesion molecules in the regulation of CNS myelination. 粘附分子在中枢神经系统髓鞘形成中的调控作用。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000161

Lisbeth S Laursen, Charles Ffrench-Constant

{"title":"Adhesion molecules in the regulation of CNS myelination.","authors":"Lisbeth S Laursen, Charles Ffrench-Constant","doi":"10.1017/S1740925X08000161","DOIUrl":"10.1017/S1740925X08000161","url":null,"abstract":"Myelination is necessary both for rapid salutatory conduction and the long-term survival of the axon. In the CNS the myelin sheath is formed by the oligodendrocytes. Each oligodendrocyte myelinates several axons and, as the number of wraps around each axon is determined precisely by the axon diameter, this requires a close, highly regulated interaction between the axons and each of the oligodendrocyte processes. Adhesion molecules are likely to play an important role in the bi-directional signalling between axon and oligodendrocyte that underlies this interaction. Here we review the current knowledge of the function of adhesion molecules in the different phases of oligodendrocyte differentiation and myelination, and discuss how the properties of these proteins defined by other cell biological systems indicates potential roles in oligodendrocytes. We show how the function of a number of different adhesion and cell-cell interaction molecules such as polysialic acid neural cell adhesion molecule, Lingo-1, Notch, neuregulin, integrins and extracellullar matrix proteins provide negative and positive signals that coordinate the formation of the myelin membrane. Compiling this information from a number of different cell biological and genetic experiments helps us to understand the pathology of multiple sclerosis and direct new areas of research that might eventually lead to potential drug targets to increase remyelination.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"367-75"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27541170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential role of the glial water channel aquaporin-4 in epilepsy. 神经胶质水通道水通道蛋白-4在癫痫中的潜在作用。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000112

Mike S Hsu, Darrin J Lee, Devin K Binder

引用次数: 33

Thursday 6 september. 9月6日星期四。

Neuron glia biology Pub Date : 2007-09-01 DOI: 10.1017/S1740925X07000531

引用次数: 0

Friday 7 september. 9月7日星期五。

Neuron glia biology Pub Date : 2007-09-01 DOI: 10.1017/S1740925X07000518

引用次数: 0

Plenary lectures and symposia. 全体演讲和专题讨论会。

Neuron glia biology Pub Date : 2007-09-01 DOI: 10.1017/S1740925X07000543

引用次数: 0