Increased sensitivity to seizures in mice lacking cellular prion protein

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dc.contributor.author Walz, Roger
dc.contributor.author Amaral, Olavo B.
dc.contributor.author Rockenbach, Isabel C.
dc.contributor.author Roesler, Rafael
dc.contributor.author Izquierdo, Ivan
dc.contributor.author Cavalheiro, Esper Abrão [UNIFESP]
dc.contributor.author Martins, Vilma R.
dc.contributor.author Brentani, Ricardo R.
dc.date.accessioned 2016-01-24T12:30:56Z
dc.date.available 2016-01-24T12:30:56Z
dc.date.issued 1999-12-01
dc.identifier http://dx.doi.org/10.1111/j.1528-1157.1999.tb01583.x
dc.identifier.citation Epilepsia. Philadelphia: Lippincott Williams & Wilkins, v. 40, n. 12, p. 1679-1682, 1999.
dc.identifier.issn 0013-9580
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/26182
dc.description.abstract Purpose: the physiologic role of the cellular prion protein (PrPc) is unknown. Mice devoid of PrPc develop normally and show only minor deficits. However, electrophysiologic and histologic alterations found in these mice suggest a possible:role fur PrPc in seizure threshold and/or epilepsy.Methods: We tested the sensitivity of PrPc knockout mice to seizures induced by single convulsant or repeated subconvulsant (kindling) doses of pentylenetetrazol (PTZ), and to status epilepticus (SE) induced by kainic acid or pilocarpine.Results. in PTZ kindling, seizure severity progressed faster in the PrPc knockout group, in which 92.8% reached stage 5 or death after 4 days of stimulation, as opposed to 38.4% in wildtype animals: After 10 injections, mortality was 85.7% among knockouts and 15.3% among controls. After a single PTZ injection (60 mg/kg), overall mortality due to seizures was 91% in knockout mice, but only 33% among wild-type animals. Pilocarpine-induced SE (320 mg/kg) caused an 86.7% mortality in knockouts, as opposed to 40% in wild-type animals. Finally, after kainic acid injections (10 mg/kg), 70% of the knockouts developed at least one severe seizure, and 50% showed repetitive seizures, whereas no wild-type animal exhibited observable seizures.Conclusions: Animals lacking cellular prion protein expression are more susceptible to seizures induced by various convulsant agents. This is perhaps the most striking alteration yet found in PrPc-null mice, who at first analysis appeared to be completely normal. A possible role for PrPc in chronic and idiopathic (familial), secondary, or cryptogenic epilepsies in humans remains to be investigated. en
dc.format.extent 1679-1682
dc.language.iso eng
dc.publisher Lippincott Williams & Wilkins
dc.relation.ispartof Epilepsia
dc.rights Acesso aberto
dc.subject prion en
dc.subject PrPc en
dc.subject seizure en
dc.subject epilepsy en
dc.subject kindling en
dc.title Increased sensitivity to seizures in mice lacking cellular prion protein en
dc.type Artigo
dc.contributor.institution Univ Fed Rio Grande Sul
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Ludwig Inst Canc Res
dc.description.affiliation Univ Fed Rio Grande Sul, ICBS, Dept Bioquim, Ctr Memoria, BR-90035003 Porto Alegre, RS, Brazil
dc.description.affiliation UNIFESP, EPM, Dept Expt Neurol, São Paulo, Brazil
dc.description.affiliation Ludwig Inst Canc Res, São Paulo, Brazil
dc.description.affiliationUnifesp UNIFESP, EPM, Dept Expt Neurol, São Paulo, Brazil
dc.identifier.doi 10.1111/j.1528-1157.1999.tb01583.x
dc.description.source Web of Science
dc.identifier.wos WOS:000084175200001



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