New mouse studies have shown that a genetic defect in the inner ear may cause hyperactivity in children with severe hearing loss. The previous explanations for childhood ADHD mainly focused on those social-environmental factors that were difficult to identify. These findings provide early evidence that ADHD may have a neurobiological basis — which opens up the possibility of discovering new targets for treatment. Jean Hébert and colleagues created a cochlear defect in the inner ear of young mice by knocking out a gene called Slc12a2 expressed in the ear. In addition to total deafness, the vestibular system of these designed mice is also compromised, and the vestibular system is crucial for balance. As can be seen in the accompanying video, these deaf and unstable standing mice are extremely hyperactive. The loss of Slc12a2 expression caused an increase in the levels of two proteins in the central part of the brain called the striatum, pERK and pCREB. When the levels of pERK and pCREB become abnormally high, the striatum will instruct the body to exercise more than it normally would, resulting in ADHD. So far, the relationship between ear dysfunction and behavior has not been explained, but this study suggests that a gene expressed in the inner ear (rather than previously thought to be in the brain) can cause ADHD. This research lays the foundation for exploring whether other sensory impairments can contribute to mental or motor disorders that are traditionally thought to originate entirely in the brain. Ear defects are linked to ADHD behavior
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