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Kv1.1 null mice have enlarged hippocampus and ventral cortex
Ann-Sophie Persson1, Eric Westman, Fu-Hua Wang
1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. a.s.persson@medisin.uio.no <a.s.persson@medisin.uio.no>
BMC Neuroscience
|January 26, 2007
Summary
Complete absence of the Kv1.1 potassium channel causes significant brain enlargement in mice. Even partial Kv1.1 deficiency does not lead to abnormal brain development.
Area of Science:
- Neuroscience
- Genetics
- Ion Channel Research
Background:
- Mutations in the Shaker-like voltage-gated potassium channel Kv1.1 are associated with episodic ataxia type 1 and temporal lobe epilepsy.
- Mice with a malfunctional, truncated Kv1.1 channel (BALB/cByJ-Kv1.1mceph/mceph) exhibit enlarged hippocampus and ventral cortex.
Purpose of the Study:
- To investigate if complete absence of Kv1.1 leads to brain enlargement similar to the mceph/mceph mouse model.
- To analyze the impact of Kv1.1 null alleles on brain structure in the BALB/cByJ background.
Main Methods:
- Transferring Kv1.1 null alleles to the BALB/cByJ mouse background.
- Utilizing in vivo 3D-magnetic resonance imaging (MRI) and volume segmentation.
- Comparing brain structures of Kv1.1 null mice, heterozygous mice (null or mceph allele), and wild-type littermates.
Main Results:
- Kv1.1 null mice displayed dramatically enlarged hippocampus and ventral cortex.
- Mice heterozygous for either the Kv1.1 null or mceph allele had normal-sized hippocampus and ventral cortex.
- The BALB/cByJ-Kv1.1mceph/mceph model also showed significant brain enlargement.
Conclusions:
- Total absence of Kv1.1 can induce excessive overgrowth of the hippocampus and ventral cortex in mice.
- A single functional Kv1.1 allele is sufficient to maintain normal brain size, indicating a dose-dependent effect.
