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dc.contributor.authorPersson, Ann-Sophie
dc.contributor.authorWestman, Eric
dc.contributor.authorWang, Fu-Hua
dc.contributor.authorKhan, Firoj H
dc.contributor.authorSpenger, Christian
dc.contributor.authorLavebratt, Catharina
dc.date.accessioned2015-10-09T01:25:42Z
dc.date.available2015-10-09T01:25:42Z
dc.date.issued2007
dc.identifier.citationBMC Neuroscience. 2007 Jan 24;8(1):10
dc.identifier.urihttp://hdl.handle.net/10852/46483
dc.description.abstractBackground Mutations in the Shaker-like voltage-gated potassium channel Kv1.1 are known to cause episodic ataxia type 1 and temporal lobe epilepsy. Mice that express a malfunctional, truncated Kv1.1 (BALB/cByJ-Kv1.1 mceph/mceph) show a markedly enlarged hippocampus and ventral cortex in adulthood. Results To determine if mice lacking Kv1.1 also develop a brain enlargement similar to mceph/mceph, we transferred Kv1.1 null alleles to the BALB/cByJ background. Hippocampus and ventral cortex was then studied using in vivo 3D-magnetic resonance imaging and volume segmentation in adult Kv1.1 null mice, BALB/cByJ-Kv1.1 mceph/mceph, BALB/cByJ-Kv1.1 mceph/+, BALB.C3HeB -Kv1.1 -/+ and wild type littermates. The Kv1.1 null brains had dramatically enlarged hippocampus and ventral cortex. Mice heterozygous for either the null allele or the mceph allele had normal-sized hippocampus and ventral cortex. Conclusion Total absence of Kv1.1 can induce excessive overgrowth of hippocampus and ventral cortex in mice with a BALB/cByJ background, while mice with one wild type Kv1.1 allele develop normal-sized brains.
dc.language.isoeng
dc.rightsPersson et al.
dc.rightsAttribution 2.0 Generic
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/
dc.titleKv1.1 null mice have enlarged hippocampus and ventral cortex
dc.typeJournal article
dc.date.updated2015-10-09T01:25:43Z
dc.creator.authorPersson, Ann-Sophie
dc.creator.authorWestman, Eric
dc.creator.authorWang, Fu-Hua
dc.creator.authorKhan, Firoj H
dc.creator.authorSpenger, Christian
dc.creator.authorLavebratt, Catharina
dc.identifier.doihttp://dx.doi.org/10.1186/1471-2202-8-10
dc.identifier.urnURN:NBN:no-50663
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/46483/1/12868_2006_Article_308.pdf
dc.type.versionPublishedVersion
cristin.articleid10


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