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2006-09-01Zeitschriftenartikel DOI: 10.1051/vetres:2006047
Propagation of scrapie in peripheral nerves after footpad infection in normal and neurotoxin exposed hamsters
dc.contributor.authorKratzel, Christine
dc.contributor.authorMai, Jessica
dc.contributor.authorMadela, Kazimierz
dc.contributor.authorBeekes, Michael
dc.contributor.authorKrüger, Dominique
dc.date.accessioned2018-05-07T13:08:00Z
dc.date.available2018-05-07T13:08:00Z
dc.date.created2009-04-30
dc.date.issued2006-09-01none
dc.date.submitted2006-05-29
dc.identifier.otherhttp://edoc.rki.de/oa/articles/reiRGh54C96No/PDF/27MTBuYbyBG6.pdf
dc.identifier.urihttp://edoc.rki.de/176904/398
dc.description.abstractAs is known from various animal models, the spread of agents causing transmissible spongiform encephalopathies (TSE) after peripheral infection affects peripheral nerves before reaching the central nervous system (CNS) and leading to a fatal end of the disease. The lack of therapeutic approaches for TSE is partially due to the limited amount of information available on the involvement of host biological compartments and processes in the propagation of the infectious agent. The in vivo model presented here can provide information on the spread of the scrapie agent via the peripheral nerves of hamsters under normal and altered axonal conditions. Syrian hamsters were unilaterally footpad (f.p.) infected with scrapie. The results of the spatiotemporal ultrasensitive immunoblot-detection of scrapie-associated prion protein (PrPSc) in serial nerve segments of both distal sciatic nerves could be interpreted as a centripetal and subsequent centrifugal neural spread of PrPSc for this route of infection. In order to determine whether this propagation is dependent on main components in the axonal cytoskeleton (e.g. neurofilaments, also relevant for the component ‘a’ of slow axonal transport mechanisms), hamsters were treated -in an additional experiment- with the neurotoxin ß,ß’-iminodiproprionitrile (IDPN) around the beginning of the scrapie infection. A comparison of the Western blot signals of PrPSc in the ipsilateral and in the subsequently affected contralateral sciatic nerve segments with the results revealed from IDPN-untreated animals at preclinical and clinical stages of the TSE disease, indicated similar amounts of PrPSc. Furthermore, the mean survival time was unchanged in both groups. This in vivo model, therefore, suggests that the propagation of PrPSc along peripheral nerves is not dependent on an intact neurofilament component of the axonal cytoskeleton. Additionally, the model indicates that the spread of PrPSc is not mediated by the slow component ‘a’ of the axonal transport mechanism.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subjectAnimalseng
dc.subjectFemaleeng
dc.subjectMaleeng
dc.subjectCricetinaeeng
dc.subjectMesocricetuseng
dc.subjectFooteng
dc.subjectNitriles/toxicityeng
dc.subjectSciatic Nerve/drug effectseng
dc.subjectSciatic Nerve/virologyeng
dc.subjectScrapie/metabolismeng
dc.subject.ddc610 Medizin
dc.titlePropagation of scrapie in peripheral nerves after footpad infection in normal and neurotoxin exposed hamsters
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-100501
dc.identifier.doi10.1051/vetres:2006047
dc.identifier.doihttp://dx.doi.org/10.25646/323
local.edoc.container-titleVeterinary Research
local.edoc.container-textThe original publication is available at www.vetres.org
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlwww.vetres.org
local.edoc.container-publisher-nameEDP Sciences
local.edoc.container-issue38
local.edoc.container-year2007

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