We are analyzing https://link.springer.com/article/10.1385/mn:27:3:325.

Title:
Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria | Molecular Neurobiology
Description:
In inflammatory, infectious, ischemic, and neurodegenerative pathologies of th central nervous system (CNS) glia become “activated” by inflammatory mediators, and express new proteins such as the inducible isoform of nitric oxide synthase (iNOS). Although these activated glia have beneficial roles, in vitro they potently kill cocultured neurons, and there is increasing evidence that they contribute to pathology in vivo. Nitric oxide (NO) from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons. NO is a potent inhibitor of mitochondrial respiration, due to reversible binding of NO to cytochrome oxidase in competition with oxygen, resulting in inhibition of energy production and sensitization to hypoxia. Activated astrocytes or microglia cause a potent inhibition of respiration in cocultured neurons due to glial NO inhibiting cytochrome oxidase within the neurons, resulting in ATP depletion and glutamate release. In some conditions, glutamate-induced neuronal death can itself be mediated by N-methyl-d-aspartate (NMDA)-receptor activation of the neuronal isoform of NO synthase (nNOS) causing mitochondrial damage. In addition NO can be converted to a number of reactive derivatives such as peroxynitrite, NO2, N2O3, and S-nitrosothiols that can kill cells in part by inhibiting mitochondrial respiration or activation of mitochondrial permeability transition, triggering neuronal apoptosis or necrosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

google, scholar, cas, pubmed, nitric, oxide, synthase, neuronal, brain, mitochondrial, res, inducible, neurosci, disease, peroxynitrite, neurochem, cell, cells, inhibition, role, brown, neurons, death, expression, glutamate, astrocytes, activation, apoptosis, rat, release, microglia, sci, dawson, production, neurotoxicity, biol, biophys, mitochondria, cytochrome, injury, neurol, biochem, inflammatory, neurodegeneration, respiration, exp, damage, chem, lett, cns,

Topics {✒️}

n-methyl-d-aspartate-mediated neurotoxicity n-methyl-d-aspartate receptors n-methyl-d-aspartate receptor n-methyl-d-aspartate tumor necrosis factor-alpha-dependent nitro-l-arginine methyl ester nitric-oxide-induced neuronal apoptosis tumor necrosis factor-alpha brown & anna bal-price month download article/chapter astrocyte-derived nitric oxide inhibited glyceraldehyde-3-phosphate dehydrogenase macrophage-induced glutamate-dependent cytotoxicity inflammation-induced dopaminergic neurodegeneration inducible nitric-oxide synthase increased nuclear factor-kappa glial-induced neuronal death nmda-induced neuronal injury nitric oxide-induced necrosis cgmp-dependent protein kinase nitric oxide-induced apoptosis experimental allergic encephalo-myelitis polymerase-1-dependent cell death microglial-produced nitric oxide nitric oxide-dependent damage blood-labyrinth barrier disruption nitric oxide biology attenuates pilocarpine-induced seizures glutamate-induced neuronal death dopaminergic sh-sy5y cells nitric oxide-mediated inhibition excitotoxin-induced caspase activation blood-brain barrier breakdown doppel-expressing mice devoid acquired immunodeficiency syndrome amyloid-beta peptide widespread peroxynitrite-mediated damage inflammatory neurodegeneration mediated neuronal excitotoxicity triggered inducible nos-ii expression related nitrogen oxides il-1-induced inos expression s-nitrosothiol-induced inhibition blood-brain-barrier dysfunction mediated neuronal apoptosis neuronal mitochondria involves nitric oxide donors subsequent excitotoxic death nadph oxidase-dependent pathway mitochondrial respiratory chain

Questions {❓}

(2002) Nitric oxide and cytochrome oxidase: substrate, inhibitor or effector?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria
         description:In inflammatory, infectious, ischemic, and neurodegenerative pathologies of th central nervous system (CNS) glia become “activated” by inflammatory mediators, and express new proteins such as the inducible isoform of nitric oxide synthase (iNOS). Although these activated glia have beneficial roles, in vitro they potently kill cocultured neurons, and there is increasing evidence that they contribute to pathology in vivo. Nitric oxide (NO) from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons. NO is a potent inhibitor of mitochondrial respiration, due to reversible binding of NO to cytochrome oxidase in competition with oxygen, resulting in inhibition of energy production and sensitization to hypoxia. Activated astrocytes or microglia cause a potent inhibition of respiration in cocultured neurons due to glial NO inhibiting cytochrome oxidase within the neurons, resulting in ATP depletion and glutamate release. In some conditions, glutamate-induced neuronal death can itself be mediated by N-methyl-d-aspartate (NMDA)-receptor activation of the neuronal isoform of NO synthase (nNOS) causing mitochondrial damage. In addition NO can be converted to a number of reactive derivatives such as peroxynitrite, NO2, N2O3, and S-nitrosothiols that can kill cells in part by inhibiting mitochondrial respiration or activation of mitochondrial permeability transition, triggering neuronal apoptosis or necrosis.
         datePublished:
         dateModified:
         pageStart:325
         pageEnd:355
         sameAs:https://doi.org/10.1385/MN:27:3:325
         keywords:
            Inflammation
            neurons
            microglia
            astrocytes
            nitric oxide
            brain
            excitotoxicity
            cell death
            Alzheimer’s disease
            Neurosciences
            Neurobiology
            Cell Biology
            Neurology
         image:
         isPartOf:
            name:Molecular Neurobiology
            issn:
               1559-1182
               0893-7648
            volumeNumber:27
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Humana Press
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Guy C. Brown
               affiliation:
                     name:University of Cambridge
                     address:
                        name:Department of Biochemistry, University of Cambridge, Cambridge, UK
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Anna Bal-Price
               affiliation:
                     name:University of Cambridge
                     address:
                        name:Department of Biochemistry, University of Cambridge, Cambridge, UK
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria
      description:In inflammatory, infectious, ischemic, and neurodegenerative pathologies of th central nervous system (CNS) glia become “activated” by inflammatory mediators, and express new proteins such as the inducible isoform of nitric oxide synthase (iNOS). Although these activated glia have beneficial roles, in vitro they potently kill cocultured neurons, and there is increasing evidence that they contribute to pathology in vivo. Nitric oxide (NO) from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons. NO is a potent inhibitor of mitochondrial respiration, due to reversible binding of NO to cytochrome oxidase in competition with oxygen, resulting in inhibition of energy production and sensitization to hypoxia. Activated astrocytes or microglia cause a potent inhibition of respiration in cocultured neurons due to glial NO inhibiting cytochrome oxidase within the neurons, resulting in ATP depletion and glutamate release. In some conditions, glutamate-induced neuronal death can itself be mediated by N-methyl-d-aspartate (NMDA)-receptor activation of the neuronal isoform of NO synthase (nNOS) causing mitochondrial damage. In addition NO can be converted to a number of reactive derivatives such as peroxynitrite, NO2, N2O3, and S-nitrosothiols that can kill cells in part by inhibiting mitochondrial respiration or activation of mitochondrial permeability transition, triggering neuronal apoptosis or necrosis.
      datePublished:
      dateModified:
      pageStart:325
      pageEnd:355
      sameAs:https://doi.org/10.1385/MN:27:3:325
      keywords:
         Inflammation
         neurons
         microglia
         astrocytes
         nitric oxide
         brain
         excitotoxicity
         cell death
         Alzheimer’s disease
         Neurosciences
         Neurobiology
         Cell Biology
         Neurology
      image:
      isPartOf:
         name:Molecular Neurobiology
         issn:
            1559-1182
            0893-7648
         volumeNumber:27
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Humana Press
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Guy C. Brown
            affiliation:
                  name:University of Cambridge
                  address:
                     name:Department of Biochemistry, University of Cambridge, Cambridge, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Anna Bal-Price
            affiliation:
                  name:University of Cambridge
                  address:
                     name:Department of Biochemistry, University of Cambridge, Cambridge, UK
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Molecular Neurobiology
      issn:
         1559-1182
         0893-7648
      volumeNumber:27
Organization:
      name:Humana Press
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Cambridge
      address:
         name:Department of Biochemistry, University of Cambridge, Cambridge, UK
         type:PostalAddress
      name:University of Cambridge
      address:
         name:Department of Biochemistry, University of Cambridge, Cambridge, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Guy C. Brown
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Biochemistry, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Anna Bal-Price
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Biochemistry, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Biochemistry, University of Cambridge, Cambridge, UK
      name:Department of Biochemistry, University of Cambridge, Cambridge, UK
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(521)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.15s.

LINK . SPRINGER . COM {}