Kv1.1 null mice have enlarged hippocampus and ventral cortex.
BMC Neurosci
; 8: 10, 2007 Jan 24.
Article
em En
| MEDLINE
| ID: mdl-17250763
ABSTRACT
BACKGROUND:
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-Kv1.1mceph/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-Kv1.1mceph/mceph, BALB/cByJ-Kv1.1mceph/+, 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.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Encefalopatias
/
Córtex Cerebral
/
Canal de Potássio Kv1.1
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Hipocampo
Limite:
Animals
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article