Alterations in mechanisms of behavioural plasticity have been proposed to be associated with various psychiatric  disorders. Potassium channels are thought to play an important role in the control of electrical signals in the brain, and therefore excitability of specific brain regions (which in turn affects plasticity). In particular, the Kv4.2 subunit has been implicated in this, through the regulation of  ction-potential back-propagation to the dendrites. However, the role that the Kv4.2 plays in anxiety or depression disorders is not well understood.

Kv4.2 knockout mice have been used to explore the effect of Kv4.2 deletion on neurological function, with evidence mostly pointing to the conclusion that the deletion of Kv4.2 can lead to exaggerated neuronal excitabilityin cortical and hippocampal regions. The cortical and hippocampal regions are strongly associated with emotion regulation, therefore  shedding light on alterations to the excitability of these regions is of high importance to studying mood disorders. In research published last week in Biology of Mood & Anxiety Disorders, Kiselycznyk et al. explore this concept further by investigating the evidence for neuropsychiatric or plasticity-related phenotypes associated with Kv4.2 knockout mice with the aim to extend the characterization of Kv4.2 KO mice in stress related phenotypes.

Kiselycznyk et al. found no evidence of neuropsychiatric or plasticity-related phenotypes in Kv4.2 knockout mice, however, they did provide further support for increased excitatory responses to novel stimuli in knockout mice. The data provides useful evidence surrounding the role of Kv4.2 in regulating neural and behavioural functions.