BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA--a supportive role for nitric oxide?
BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA--a supportive role for nitric oxide?
Loading...
Date
2001
Authors
Editors
Journal ISSN
Electronic ISSN
ISBN
Bibliographical data
Publisher
Series
URI (citable link)
DOI (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
Neurobiology of Disease ; 8 (2001), 1. - pp. 103-113. - ISSN 0969-9961
Abstract
The death of neurons and the limited ability to activate growth-associated genes prevent the restoration of lesioned fiber tracts in the adult mammalian CNS. Here, we characterized the effects of the survival-promoting neurotrophin brain-derived neurotrophic factor (BDNF) on mRNA expression of GAP-43, L1, TAG-1, and SC-1 in axotomized and regenerating rat retinal ganglion cells (RGCs). BDNF led to de novo upregulation of TAG-1 mRNA in axotomized RGCs and to a threefold increase in the number of GAP-43 and L1 mRNA-expressing RGCs. SC-1 expression remained unchanged. However, BDNF did not improve long-distance axon regeneration into a peripheral nerve graft. Surprisingly, potentiating BDNF-mediated neuroprotection by simultaneous administration of a spin trap or a NOS inhibitor counteracted the BDNF-induced growth-associated gene expression. This led us to hypothesize that the BDNF effects on GAP-43, L1, and TAG-1 mRNA expression are mediated by a NO-dependent mechanism. In summary, our data support the idea that survival and axon regeneration of lesioned CNS neurons can be regulated independently.
Summary in another language
Subject (DDC)
570 Biosciences, Biology
Keywords
Conference
Review
undefined / . - undefined, undefined. - (undefined; undefined)
Cite This
ISO 690
KLÖCKER, Nikolaj, Marion JUNG, Claudia STÜRMER, Mathias BÄHR, 2001. BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA--a supportive role for nitric oxide?. In: Neurobiology of Disease. 8(1), pp. 103-113. ISSN 0969-9961. Available under: doi: 10.1006/nbdi.2000.0329BibTex
@article{Klocker2001-02incre-17474, year={2001}, doi={10.1006/nbdi.2000.0329}, title={BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA--a supportive role for nitric oxide?}, number={1}, volume={8}, issn={0969-9961}, journal={Neurobiology of Disease}, pages={103--113}, author={Klöcker, Nikolaj and Jung, Marion and Stürmer, Claudia and Bähr, Mathias} }
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/123456789/17474"> <dc:creator>Jung, Marion</dc:creator> <dcterms:title>BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA--a supportive role for nitric oxide?</dcterms:title> <foaf:homepage rdf:resource="http://localhost:8080/"/> <dc:contributor>Stürmer, Claudia</dc:contributor> <dc:rights>terms-of-use</dc:rights> <dc:creator>Bähr, Mathias</dc:creator> <dcterms:issued>2001-02</dcterms:issued> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-01-18T15:50:46Z</dc:date> <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/17474/2/Kloecker_174748.pdf"/> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-01-18T15:50:46Z</dcterms:available> <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/17474/2/Kloecker_174748.pdf"/> <dcterms:bibliographicCitation>Publ. in: Neurobiology of Disease ; 8 (2001), 1. - S. 103-113</dcterms:bibliographicCitation> <dcterms:abstract xml:lang="deu">The death of neurons and the limited ability to activate growth-associated genes prevent the restoration of lesioned fiber tracts in the adult mammalian CNS. Here, we characterized the effects of the survival-promoting neurotrophin brain-derived neurotrophic factor (BDNF) on mRNA expression of GAP-43, L1, TAG-1, and SC-1 in axotomized and regenerating rat retinal ganglion cells (RGCs). BDNF led to de novo upregulation of TAG-1 mRNA in axotomized RGCs and to a threefold increase in the number of GAP-43 and L1 mRNA-expressing RGCs. SC-1 expression remained unchanged. However, BDNF did not improve long-distance axon regeneration into a peripheral nerve graft. Surprisingly, potentiating BDNF-mediated neuroprotection by simultaneous administration of a spin trap or a NOS inhibitor counteracted the BDNF-induced growth-associated gene expression. This led us to hypothesize that the BDNF effects on GAP-43, L1, and TAG-1 mRNA expression are mediated by a NO-dependent mechanism. In summary, our data support the idea that survival and axon regeneration of lesioned CNS neurons can be regulated independently.</dcterms:abstract> <dc:contributor>Klöcker, Nikolaj</dc:contributor> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:contributor>Jung, Marion</dc:contributor> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/17474"/> <dc:creator>Stürmer, Claudia</dc:creator> <dc:creator>Klöcker, Nikolaj</dc:creator> <dc:language>deu</dc:language> <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/> <dc:contributor>Bähr, Mathias</dc:contributor> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/> </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