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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. ANK3 is a leading bipolar disorder BD candidate gene in humans and provides a unique opportunity for studying epilepsy-BD comorbidity. Previous studies showed that deletion of Ankb , a BD-associated variant of Ank3 in mice leads to increased firing threshold and diminished action potential dynamic range of parvalbumin PV interneurons and absence epilepsy, thus providing a biological mechanism linking epilepsy and BD.
To explore the behavioral overlap of these disorders, we characterized behavioral patterns of Ankb KO mice during overnight home-cage activity and examined network activity during these behaviors using paired video and EEG recordings. During sleep, increased slow gamma power correlated with decreased time spent in the rapid eye movement REM stage of sleep. We also found that Ankb KO mice were hyperactive and exhibited a repetitive behavior phenotype that co-occurred with increased slow gamma power.
Our results identify a novel EEG biomarker associating Ank3 genetic variation with BD and epilepsy and suggest modulation of gamma oscillations as a potential therapeutic target. Epilepsy and bipolar disorder BD are chronic, episodic, and debilitating disorders that often lead to suicide.
Reciprocally, people with BD are at a four-fold increased risk of developing epilepsy [ 2 , 3 , 4 ]. In addition to these shared features and bidirectional comorbidity, anticonvulsant medications are often used to effectively treat BD, and kindling effects seen in BD are hypothesized to be related to kindling in epilepsy [ 5 ].
