摘要：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- Kv1.1 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.
