The inner ear has two structures, the cochlea and the vestibular system.
Behavioral problems are typically believed to originate in the brain. However, a new study by researchers at Albert Einstein College of Medicine at Yeshiva University has revealed that inner-ear issues might actually have a direct neurological effect that increases hyperactivity. The study was conducted on mice and implicated two different brain proteins in the process which provides potential targets for intervention.
For many years, scientists have noticed that children and adolescents with severe inner-ear disorders, particularly those that effect hearing and balance, also exhibit behavioral issues like hyperactivity. Until now, no one has been able to determine if the two were linked in some way.
“Our study provides the first evidence that a sensory impairment, such as inner-ear dysfunction, can induce specific molecular changes in the brain that cause maladaptive behaviors traditionally considered to originate exclusively in the brain,” said study leader Jean M. Hebert, Ph.D., professor in the Dominick P. Purpura Department of Neuroscience and of genetics at Albert Einstein College of Medicine.
The inner ear has two structures, the cochlea, which is responsible for hearing, and the vestibular system, which is responsible for balance. Inner-ear problems are usually a result of genetic defects but can also be caused by infection or injury.
The idea for this study came when Michelle W. Antoine, a then Ph.D. student at Einstein, noticed that some of the mice in Dr. Herbert’s lab were unusually active, presenting almost continuous movement and chasing their tails in a circular pattern. Close investigation revealed that the mice had severe inner-ear defects and were profoundly deaf.
“We then realized that these mice provided a good opportunity to study the relationship between inner-ear dysfunction and behavior,” said Dr. Hebert.
Researchers determined that the inner-ear problems were a result of a mutation in a gene known as Slc12a2. this gene is responsible for transporting sodium, potassium and chloride molecules to various tissues, including the inner ear and the central nervous system.
To determine if the gene mutation was actually connected to the animals’ hyperactivity, researchers selectively deleted the Slc2a2 gene from either the inner ear of healthy mice, parts of the brain that control movement or the whole central nervous system. What they discovered was that when the gene was deleted from the gene in the inner ear, increased locomotor activity could be observed.
“Our study also raises the intriguing possibility that other sensory impairments not associated with inner-ear defects could cause or contribute to psychiatric or motor disorders that are now considered exclusively of cerebral origin,” said Dr. Hebert. “This is an area that has not been well studied.”
The study’s findings can be found in the online edition of Science.
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