Neuron glia biology最新文献_第10页

Cell contact-inhibition signaling as part of wound-healing processes in brain. 细胞接触抑制信号作为脑创伤愈合过程的一部分。

Neuron glia biology Pub Date : 2008-02-01 Epub Date: 2008-11-13 DOI: 10.1017/S1740925X09000039

Ximena A Lanosa, Jorge A Colombo

引用次数: 11

Neuron glia biology Pub Date : 2008-02-01 DOI: 10.1017/S1740925X09000040

R. Fields

引用次数: 1

Glutamate elicits release of BDNF from basal forebrain astrocytes in a process dependent on metabotropic receptors and the PLC pathway. 谷氨酸诱导基底前脑星形胶质细胞释放BDNF，这一过程依赖于代谢受体和PLC通路。

Neuron glia biology Pub Date : 2008-02-01 DOI: 10.1017/S1740925X09000052

Ying Y Jean, Lauren D Lercher, Cheryl F Dreyfus

{"title":"Glutamate elicits release of BDNF from basal forebrain astrocytes in a process dependent on metabotropic receptors and the PLC pathway.","authors":"Ying Y Jean, Lauren D Lercher, Cheryl F Dreyfus","doi":"10.1017/S1740925X09000052","DOIUrl":"https://doi.org/10.1017/S1740925X09000052","url":null,"abstract":"A key neurotrophin responsible for the survival and function of basal forebrain (BF) cholinergic neurons is brain-derived neurotrophic factor (BDNF). A number of studies now indicate that a source of this factor may be BF astrocytes. This study was designed to define the role of BF-astrocyte-derived BDNF on cholinergic neurons. Moreover, it investigated regulatory events that modulate BDNF content and release. In initial work BDNF derived from BF-astrocyte-conditioned medium (ACM) was found to increase both numbers of BF acetylcholinesterase (AChE+) cholinergic neurons and the cholinergic synthetic enzyme choline acetyltransferase (ChAT). Western blots, immunocytochemistry and pharmacological inhibition studies revealed that glutamate, through group I metabotropic glutamate receptors (mGluR), increases the intracellular levels of BDNF in BF astrocytes in culture, as well as its release. Furthermore, the release of BDNF is mediated by the actions of PLC, IP3 and internal stores of Ca2+. These results suggest that BF astrocytes serve as local sources of BDNF for cholinergic neurons, and that they may be regulated as such by the neuronal signal, glutamate, through the mediation of group I metabotropic receptors and the PLC pathway.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"4 1","pages":"35-42"},"PeriodicalIF":0.0,"publicationDate":"2008-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X09000052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28106666","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: 98

Interaction between glutamate signalling and immune attack in damaging oligodendrocytes. 谷氨酸信号与免疫攻击在损伤少突胶质细胞中的相互作用。

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000033

Carlos Matute

{"title":"Interaction between glutamate signalling and immune attack in damaging oligodendrocytes.","authors":"Carlos Matute","doi":"10.1017/S1740925X08000033","DOIUrl":"https://doi.org/10.1017/S1740925X08000033","url":null,"abstract":"Glutamate is the principal excitatory neurotransmitter in the CNS, but it is also a potent neurotoxin that can kill nerve cells. Glutamate damages oligodendrocytes, like neurons, by excitotoxicity which is caused by sustained activation of AMPA, kainate and NMDA receptors. Glutamate excitotoxicity depends entirely on Ca(2+) overload of the cytoplasm and can be initiated by disruption of glutamate homeostasis. Thus, inhibition of glutamate uptake in isolated oligodendrocytes in vitro and in the optic nerve in vivo, is sufficient to trigger cell death which is prevented by glutamate receptor antagonists. In turn, activated, but not resting microglia, can compromise glutamate homeostasis and induce oligodendrocyte excitotoxicity, which is attenuated either by AMPA/kainate antagonists or by the blockade of the system x(c)- antiporter present in microglia. By contrast, non-lethal, brief, activation of glutamate receptors in oligodendrocytes rapidly sensitizes these cells to complement attack. Intriguingly, these effects are exclusively mediated by kainate receptors which induce Ca(2+) overload of the cytosol and the generation of reactive oxygen species. In conjunction, these observations reveal novel mechanisms by which neuroinflammation alters glutamate homeostasis and triggers oligodendrocyte death. Conversely, they also show how glutamate signaling in oligodendrocytes might induce immune attack. In both instances direct activation of glutamate receptors present in oligodendrocytes plays a pivotal role in either initiating or executing death signals, which might be relevant to the pathogenesis of white matter disorders.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"281-5"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X08000033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27543403","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: 25

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

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":"https://doi.org/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://sci-hub-pdf.com/10.1017/S1740925X0800015X","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: 109

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

Interactions of Sox10 and Egr2 in myelin gene regulation. Sox10 和 Egr2 在髓鞘基因调控中的相互作用

Neuron glia biology Pub Date : 2007-11-01 DOI: 10.1017/S1740925X08000173

Erin A Jones, Sung-Wook Jang, Gennifer M Mager, Li-Wei Chang, Rajini Srinivasan, Nolan G Gokey, Rebecca M Ward, Rakesh Nagarajan, John Svaren

{"title":"Interactions of Sox10 and Egr2 in myelin gene regulation.","authors":"Erin A Jones, Sung-Wook Jang, Gennifer M Mager, Li-Wei Chang, Rajini Srinivasan, Nolan G Gokey, Rebecca M Ward, Rakesh Nagarajan, John Svaren","doi":"10.1017/S1740925X08000173","DOIUrl":"10.1017/S1740925X08000173","url":null,"abstract":"Myelination in the PNS is accompanied by a large induction of the myelin protein zero (Mpz) gene to produce the most abundant component in peripheral myelin. Analyses of knockout mice have shown that the EGR2/Krox20 and SOX10 transcription factors are required for Mpz expression. Our recent work has shown that the dominant EGR2 mutations associated with human peripheral neuropathies cause disruption of EGR2/SOX10 synergy at specific sites, including a conserved enhancer element in the first intron of the Mpz gene. Further investigation of Egr2/Sox10 interactions reveals that activation of the Mpz intron element by Egr2 requires both Sox10-binding sites. In addition, both Egr1 and Egr3 cooperate with Sox10 to activate this element, which indicates that this capacity is conserved among Egr family members. Finally, a conserved composite structure of Egr2/Sox10-binding sites in the genes encoding Mpz, myelin-associated glycoprotein and myelin basic protein genes was used to screen for similar modules in other myelin genes, revealing a potential regulatory element in the periaxin gene. Overall, these results elucidate a working model for developmental regulation of Mpz expression, several facets of which extend to regulation of other peripheral myelin genes.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"3 4","pages":"377-87"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605513/pdf/nihms77039.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27541172","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":"https://doi.org/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":"https://sci-hub-pdf.com/10.1017/S1740925X0800001X","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: 27