We are analyzing https://link.springer.com/article/10.1007/s00726-006-0396-9.

Title:
Taurine increases mitochondrial buffering of calcium: role in neuroprotection | Amino Acids
Description:
We have determined the role of mitochondria in the sequestration of calcium after stimulation of cerebellar granule cells with glutamate. In addition we have evaluated the neuroprotective role of taurine in excitotoxic cell death. Mitochondrial inhibitors were used to determine the calcium buffering capacity of mitochondria, as well as how taurine regulates the ability of mitochondria to buffer intracellular calcium during glutamate depolarization and excitotoxicity. We report here that pre-treatment of cerebellar granule cells with taurine (1 mM, 24 h) significantly counteracted glutamate excitotoxicity. The neuroprotective role of taurine was mediated through regulation of cytoplasmic free calcium ([Ca2+] i ), and intra-mitochondrial calcium homeostasis, as determined by fluo-3 and 45Ca2+-uptake. Furthermore, the overall mitochondrial function was increased in the presence of taurine, as assessed by rhodamine accumulation into mitochondria and total cellular ATP levels. We specifically tested the hypothesis that taurine reduces glutamate excitotoxicity through both the enhancement of mitochondrial function and the regulation of intracellular (cytoplasmic and intra-mitochondrial) calcium homeostasis. The role of taurine in modulating mitochondrial calcium homeostasis could be of particular importance under pathological conditions that are characterized by excessive calcium overloads. Taurine may serve as an endogenous neuroprotective molecule against brain insults.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Telecommunications
Science

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 don't see any clear sign of profit-making.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

google, scholar, article, cas, pubmed, calcium, taurine, mitochondrial, glutamate, neurosci, role, mitochondria, excitotoxicity, cells, cell, homeostasis, neuronal, lett, cerebellar, amino, acids, idrissi, granule, pharmacol, rat, febs, privacy, cookies, content, intracellular, brain, access, neurochem, function, information, publish, search, death, uptake, neurons, related, biol, nicholls, cultured, res, effects, data, log, journal, research,

Topics {✒️}

article google scholar month download article/chapter strychnine-insensitive glycine/nmda sites short-duration glutamate challenge intra-mitochondrial calcium homeostasis cerebellar granule cells taurine-sensitive chloride channels glutamate-induced deregulation full article pdf calcium buffering capacity stabilizing calcium homeostasis stauderman ma varney neuronal calcium recovery induce neuronal death cardiac muscle cells privacy choices/manage cookies excitotoxic cell death carabez rj huxtable programmed cell death acute glutamate excitotoxicity glutamate excitotoxicity studied glutamate-stimulated neurons subsequent neuronal degeneration brustovetsky jm dubinsky sadée jm quillan central nervous system abdeslem el idrissi independent mitochondrial damage dyak28xnt1squ70%3d 10 dyak2cxhvvyrsrs%3d 10 taurine binding sites excessive calcium overloads mediates calcium influx calcium ion uptake buffer intracellular calcium plasma membrane ca2+/ structurally related analogues amino acids 34 mitochondrial membrane potential mitochondria transport calcium cytosolic ca2+ imaging cortical circuit formation neurotoxic glutamate treatment intracellular ca2+ network zajdela hepatoma mitochondrial article log cerebellar cells taurine transport antagonist cytoplasmic free calcium calcium homeostasis

Questions {❓}

B Lucas-Heron B Le Ray N Schmitt (1995) Does calmitine, a protein specific for the mitochondrial matrix of skeletal muscle, play a key role in mitochondrial function?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Taurine increases mitochondrial buffering of calcium: role in neuroprotection
         description:We have determined the role of mitochondria in the sequestration of calcium after stimulation of cerebellar granule cells with glutamate. In addition we have evaluated the neuroprotective role of taurine in excitotoxic cell death. Mitochondrial inhibitors were used to determine the calcium buffering capacity of mitochondria, as well as how taurine regulates the ability of mitochondria to buffer intracellular calcium during glutamate depolarization and excitotoxicity. We report here that pre-treatment of cerebellar granule cells with taurine (1 mM, 24 h) significantly counteracted glutamate excitotoxicity. The neuroprotective role of taurine was mediated through regulation of cytoplasmic free calcium ([Ca2+] i ), and intra-mitochondrial calcium homeostasis, as determined by fluo-3 and 45Ca2+-uptake. Furthermore, the overall mitochondrial function was increased in the presence of taurine, as assessed by rhodamine accumulation into mitochondria and total cellular ATP levels. We specifically tested the hypothesis that taurine reduces glutamate excitotoxicity through both the enhancement of mitochondrial function and the regulation of intracellular (cytoplasmic and intra-mitochondrial) calcium homeostasis. The role of taurine in modulating mitochondrial calcium homeostasis could be of particular importance under pathological conditions that are characterized by excessive calcium overloads. Taurine may serve as an endogenous neuroprotective molecule against brain insults.
         datePublished:2006-09-08T00:00:00Z
         dateModified:2006-09-08T00:00:00Z
         pageStart:321
         pageEnd:328
         sameAs:https://doi.org/10.1007/s00726-006-0396-9
         keywords:
            Keywords: Taurine – Excitotoxicity – Calcium homeostasis – Mitochondria
            Biochemistry
            general
            Analytical Chemistry
            Biochemical Engineering
            Life Sciences
            Proteomics
            Neurobiology
         image:
         isPartOf:
            name:Amino Acids
            issn:
               1438-2199
               0939-4451
            volumeNumber:34
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:A. El Idrissi
               affiliation:
                     name:College of Staten Island of the City University of New York
                     address:
                        name:Department of Biology and Center for Developmental Neuroscience, College of Staten Island of the City University of New York, New York, U.S.A.
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Taurine increases mitochondrial buffering of calcium: role in neuroprotection
      description:We have determined the role of mitochondria in the sequestration of calcium after stimulation of cerebellar granule cells with glutamate. In addition we have evaluated the neuroprotective role of taurine in excitotoxic cell death. Mitochondrial inhibitors were used to determine the calcium buffering capacity of mitochondria, as well as how taurine regulates the ability of mitochondria to buffer intracellular calcium during glutamate depolarization and excitotoxicity. We report here that pre-treatment of cerebellar granule cells with taurine (1 mM, 24 h) significantly counteracted glutamate excitotoxicity. The neuroprotective role of taurine was mediated through regulation of cytoplasmic free calcium ([Ca2+] i ), and intra-mitochondrial calcium homeostasis, as determined by fluo-3 and 45Ca2+-uptake. Furthermore, the overall mitochondrial function was increased in the presence of taurine, as assessed by rhodamine accumulation into mitochondria and total cellular ATP levels. We specifically tested the hypothesis that taurine reduces glutamate excitotoxicity through both the enhancement of mitochondrial function and the regulation of intracellular (cytoplasmic and intra-mitochondrial) calcium homeostasis. The role of taurine in modulating mitochondrial calcium homeostasis could be of particular importance under pathological conditions that are characterized by excessive calcium overloads. Taurine may serve as an endogenous neuroprotective molecule against brain insults.
      datePublished:2006-09-08T00:00:00Z
      dateModified:2006-09-08T00:00:00Z
      pageStart:321
      pageEnd:328
      sameAs:https://doi.org/10.1007/s00726-006-0396-9
      keywords:
         Keywords: Taurine – Excitotoxicity – Calcium homeostasis – Mitochondria
         Biochemistry
         general
         Analytical Chemistry
         Biochemical Engineering
         Life Sciences
         Proteomics
         Neurobiology
      image:
      isPartOf:
         name:Amino Acids
         issn:
            1438-2199
            0939-4451
         volumeNumber:34
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:A. El Idrissi
            affiliation:
                  name:College of Staten Island of the City University of New York
                  address:
                     name:Department of Biology and Center for Developmental Neuroscience, College of Staten Island of the City University of New York, New York, U.S.A.
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Amino Acids
      issn:
         1438-2199
         0939-4451
      volumeNumber:34
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:College of Staten Island of the City University of New York
      address:
         name:Department of Biology and Center for Developmental Neuroscience, College of Staten Island of the City University of New York, New York, U.S.A.
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:A. El Idrissi
      affiliation:
            name:College of Staten Island of the City University of New York
            address:
               name:Department of Biology and Center for Developmental Neuroscience, College of Staten Island of the City University of New York, New York, U.S.A.
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Biology and Center for Developmental Neuroscience, College of Staten Island of the City University of New York, New York, U.S.A.
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(136)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

3.68s.

LINK . SPRINGER . COM {}