Pentylenetetrazol-kindling in mice overexpressing heat shock protein 70

Απλή σελίδα τεκμηρίου
dc.contributor.authorAmmon-Treiber, S.en
dc.contributor.authorGrecksch, G.en
dc.contributor.authorAngelidis, C.en
dc.contributor.authorVezyraki, P.en
dc.contributor.authorHollt, V.en
dc.contributor.authorBecker, A.en
dc.date.accessioned2015-11-24T18:59:46Z
dc.date.available2015-11-24T18:59:46Z
dc.identifier.issn0028-1298-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/19407
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectConvulsants/administration & dosage/toxicityen
dc.subjectDisease Models, Animalen
dc.subjectDose-Response Relationship, Drugen
dc.subjectHSP70 Heat-Shock Proteins/genetics/*physiologyen
dc.subjectHippocampus/drug effects/metabolismen
dc.subjectInjections, Intraperitonealen
dc.subjectKindling, Neurologic/*drug effects/physiologyen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectMice, Inbred CBAen
dc.subjectMice, Transgenicen
dc.subjectPentylenetetrazole/administration & dosage/*toxicityen
dc.subjectSeizures/chemically induced/physiopathologyen
dc.titlePentylenetetrazol-kindling in mice overexpressing heat shock protein 70en
heal.abstractKindling induced by the convulsant pentylenetetrazol (PTZ) is an accepted model of primary generalized epilepsy. Because seizures represent a strong distressing stimulus, stress-induced proteins such as heat shock proteins might counteract the pathology of increased neuronal excitation. Therefore, the aim of the present study was to determine whether PTZ kindling outcome parameters are influenced by heat shock protein 70 (Hsp70) overexpression in Hsp70 transgenic mice as compared to the respective wild-type mice. Kindling was performed by nine intraperitoneal injections of PTZ (ED(16) for induction of clonic-tonic seizures, every 48 h); control animals received saline instead of PTZ. Seven days after the final injection, all mice received a PTZ challenge dose. Outcome parameters included evaluation of seizure stages and overall survival rates. In addition, histopathological findings such as cell number in hippocampal subfields CA1 and CA3 were determined. The onset of the highest convulsion stage was delayed in Hsp70 transgenic mice as compared to wild-type mice, and overall survival during kindling was improved in Hsp70 transgenic mice as compared to wild-type mice. In addition, a challenge dose after termination of kindling produced less severe seizures in Hsp70 transgenic mice than in wild-type mice. PTZ kindling did not result in significant subsequent neuronal cell loss in CA1 or CA3 neither in wild-type mice nor in the Hsp70 transgenic mice. The results of the present experiments clearly demonstrate that overexpression of Hsp70 exerts protective effects regarding seizure severity and overall survival during PTZ kindling. In addition, the decreased seizure severity in Hsp70 transgenic mice after a challenge dose suggests an interference of Hsp70 with the developmental component of kindling.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1007/s00210-007-0143-0-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17333130-
heal.identifier.secondaryhttp://www.springerlink.com/content/nj28w767604m8n20/fulltext.pdf-
heal.journalNameNaunyn Schmiedebergs Arch Pharmacolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2007-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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