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K v 10.1 (Eag1), member of the K v 10 family of voltage-gated potassium channels, is preferentially expressed in adult brain. The aim of the present study was to unravel the functional role of K v 10.1 in the brain by generating knockout mice, where the voltage sensor and pore region of K v 10.1 were removed to render non-functional proteins through deletion of exon 7 of the KCNH1 gene using the ‘3 Lox P strategy’. K v 10.1-deficient mice show no obvious alterations during embryogenesis and develop normally to adulthood; cortex, hippocampus and cerebellum appear anatomically normal. Other tests, including general health screen, sensorimotor functioning and gating, anxiety, social behaviour, learning and memory did not show any functional aberrations in K v 10.1 null mice. K v 10.1 null mice display mild hyperactivity and longer-lasting haloperidol-induced catalepsy, but there was no difference between genotypes in amphetamine sensitization and withdrawal, reactivity to apomorphine and haloperidol in the prepulse inhibition tests or to antidepressants in the haloperidol-induced catalepsy. Furthermore, electrical properties of K v 10.1 in cerebellar Purkinje cells did not show any difference between genotypes. Bearing in mind that K v 10.1 is overexpressed in over 70% of all human tumours and that its inhibition leads to a reduced tumour cell proliferation, the fact that deletion of K v 10.1 does not show a marked phenotype is a prerequisite for utilizing K v 10.1 blocking and/or reduction techniques, such as siRNA, to treat cancer.

Behavioural and functional characterization of K v 10.1 (Eag1) knockout mice