Publikation:

Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice

Lade...
Vorschaubild

Dateien

cdd_98_app.pdf
cdd_98_app.pdfGröße: 843.12 KBDownloads: 287

Datum

1998

Autor:innen

Steinbach, Joachim P.
Müller, Ulrike
Li, Zhi-Wei
Aguzzi, Adriano

Herausgeber:innen

Kontakt

ISSN der Zeitschrift

Electronic ISSN

ISBN

Bibliografische Daten

Verlag

Schriftenreihe

Auflagebezeichnung

DOI (zitierfähiger Link)
ArXiv-ID

Internationale Patentnummer

Angaben zur Forschungsförderung

Projekt

Open Access-Veröffentlichung
Open Access Green
Core Facility der Universität Konstanz

Gesperrt bis

Titel in einer weiteren Sprache

Publikationstyp
Zeitschriftenartikel
Publikationsstatus
Published

Erschienen in

Journal of Cell Death and Differentiation. 1998, 5(10), pp. 858-866

Zusammenfassung

Secreted forms of the β-amyloid precursor protein (β-APP) have neuroprotective properties in vitro and may be involved in the containment of neuronal excitation. To test whether loss of secreted forms of β-APP (sAPPs) may enhance excitotoxic responses, we injected mice homozygous for a targeted mutation of the β-APP gene (β-APP∆/∆) intraperitoneally with kainic acid. We found that in these mice, kainic acid induced seizures initiated earlier, and acute mortality was enhanced compared to isogenic wild-type mice independently from the callosal agenesis phenotype observed to occur at increased frequency in APP mutant mice. Expression of c-fos in cortex and cingulate gyrus was enhanced in β-APP∆/∆ mice, although the amount of structural damage and apoptosis in the hippocampal pyramidal cell layer and cortex was similar to that of controls. When cerebellar granule cell cultures and cortical neuronal cultures were challenged with glutamate receptor agonists, the rates of cell death and apoptosis of β-APP∆/∆ mice were indistinguishable from those of controls. Therefore, deficiency of sAPPs causes facilitation of seizure activity in the absence of enhanced cell death. Since enhanced seizures were observed also in mice homozygous for a deletion of the entire β-APP gene, this phenotype results from a loss of APP rather than from a dominant effect of APP∆.

Zusammenfassung in einer weiteren Sprache

Fachgebiet (DDC)
570 Biowissenschaften, Biologie

Schlagwörter

Alzheimer's disease, β-amyloid precursor protein, β- APP deficient mice, kainic acid, neuronal cultures, excitotoxicity c-fos, apoptosis

Konferenz

Rezension
undefined / . - undefined, undefined

Forschungsvorhaben

Organisationseinheiten

Zeitschriftenheft

Zugehörige Datensätze in KOPS

Zitieren

ISO 690STEINBACH, Joachim P., Ulrike MÜLLER, Marcel LEIST, Zhi-Wei LI, Pierluigi NICOTERA, Adriano AGUZZI, 1998. Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice. In: Journal of Cell Death and Differentiation. 1998, 5(10), pp. 858-866
BibTex
@article{Steinbach1998Hyper-8115,
  year={1998},
  title={Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice},
  number={10},
  volume={5},
  journal={Journal of Cell Death and Differentiation},
  pages={858--866},
  author={Steinbach, Joachim P. and Müller, Ulrike and Leist, Marcel and Li, Zhi-Wei and Nicotera, Pierluigi and Aguzzi, Adriano}
}
RDF
<rdf:RDF
    xmlns:dcterms="http://purl.org/dc/terms/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
    xmlns:bibo="http://purl.org/ontology/bibo/"
    xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#"
    xmlns:foaf="http://xmlns.com/foaf/0.1/"
    xmlns:void="http://rdfs.org/ns/void#"
    xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > 
  <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/8115">
    <dc:creator>Li, Zhi-Wei</dc:creator>
    <dc:language>eng</dc:language>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:40:44Z</dcterms:available>
    <dc:contributor>Müller, Ulrike</dc:contributor>
    <dc:format>application/pdf</dc:format>
    <dc:contributor>Aguzzi, Adriano</dc:contributor>
    <dc:creator>Müller, Ulrike</dc:creator>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:creator>Steinbach, Joachim P.</dc:creator>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8115/1/cdd_98_app.pdf"/>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8115/1/cdd_98_app.pdf"/>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dc:contributor>Nicotera, Pierluigi</dc:contributor>
    <dc:rights>terms-of-use</dc:rights>
    <dc:contributor>Steinbach, Joachim P.</dc:contributor>
    <dc:creator>Nicotera, Pierluigi</dc:creator>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:abstract xml:lang="eng">Secreted forms of the β-amyloid precursor protein (β-APP) have neuroprotective properties in vitro and may be involved in the containment of neuronal excitation. To test whether loss of secreted forms of β-APP (sAPPs) may enhance excitotoxic responses, we injected mice homozygous for a targeted mutation of the β-APP gene (β-APP∆/∆) intraperitoneally with kainic acid. We found that in these mice, kainic acid induced seizures initiated earlier, and acute mortality was enhanced compared to isogenic wild-type mice independently from the callosal agenesis phenotype observed to occur at increased frequency in APP mutant mice. Expression of c-fos in cortex and cingulate gyrus was enhanced in β-APP∆/∆ mice, although the amount of structural damage and apoptosis in the hippocampal pyramidal cell layer and cortex was similar to that of controls. When cerebellar granule cell cultures and cortical neuronal cultures were challenged with glutamate receptor agonists, the rates of cell death and apoptosis of β-APP∆/∆ mice were indistinguishable from those of controls. Therefore, deficiency of sAPPs causes facilitation of seizure activity in the absence of enhanced cell death. Since enhanced seizures were observed also in mice homozygous for a deletion of the entire β-APP gene, this phenotype results from a loss of APP rather than from a dominant effect of APP∆.</dcterms:abstract>
    <dc:contributor>Li, Zhi-Wei</dc:contributor>
    <dc:creator>Leist, Marcel</dc:creator>
    <dcterms:title>Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice</dcterms:title>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:40:44Z</dc:date>
    <dcterms:issued>1998</dcterms:issued>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dcterms:bibliographicCitation>First publ. in: Journal of Cell Death and Differentiation 5 (1998), 10, pp. 858-866</dcterms:bibliographicCitation>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/8115"/>
    <dc:creator>Aguzzi, Adriano</dc:creator>
  </rdf:Description>
</rdf:RDF>

Interner Vermerk

xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter

Kontakt
URL der Originalveröffentl.

Prüfdatum der URL

Prüfungsdatum der Dissertation

Finanzierungsart

Kommentar zur Publikation

Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Nein
Begutachtet
Diese Publikation teilen