Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice
Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice
Loading...
Date
1998
Authors
Editors
Journal ISSN
Electronic ISSN
ISBN
Bibliographical data
Publisher
Series
URI (citable link)
International patent number
Link to the license
EU project number
Project
Open Access publication
Collections
Title in another language
Publication type
Journal article
Publication status
Published in
Journal of Cell Death and Differentiation ; 5 (1998), 10. - pp. 858-866
Abstract
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∆.
Summary in another language
Subject (DDC)
570 Biosciences, Biology
Keywords
Alzheimer's disease,β-amyloid precursor protein,β- APP deficient mice,kainic acid,neuronal cultures,excitotoxicity c-fos,apoptosis
Conference
Review
undefined / . - undefined, undefined. - (undefined; undefined)
Cite This
ISO 690
STEINBACH, 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. 5(10), pp. 858-866BibTex
@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>
Internal note
xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter
Examination date of dissertation
Method of financing
Comment on publication
Alliance license
Corresponding Authors der Uni Konstanz vorhanden
International Co-Authors
Bibliography of Konstanz
No