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BMC Neurosci. 2007 Jan 24;8:10.

Kv1.1 null mice have enlarged hippocampus and ventral cortex.

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  • 1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. a.s.persson@medisin.uio.no <a.s.persson@medisin.uio.no>



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.


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.


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.

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