Health and fitness news - PUNCH

October 14, 2013 by Agency Reporter

Hyperactivity linked to inner ear defect

When hyperactivity is found in children with severe hearing loss, it is often assumed to stem from frustrations they have communicating or socialising.

But a new study says a genetic defect in the inner ear may also play a role in causing hyperactive behavior, suggesting that at least in some cases, hyperactivity can have a neurobiological root.

Researchers at the Albert Einstein College of Medicine in the Bronx caused inner-ear defects in young mice by knocking out a gene called Slc12a2, causing a loss of hearing and sense of balance.

But the removal of the gene also resulted in higher levels of two proteins, pERK and pCREB, in the striatum, a part of the brain that helps regulate motor functions.

The mice then displayed hyperactive behavior, like running rapidly in a circle.

Suspecting that the higher protein levels were causing the behavior, the researchers lowered them. With normal levels of pERK and pCREB restored, the mice’s behavior returned to normal.

Precisely which neural pathway from the ear to the brain was active in this case is not yet clear, said the study’s lead author, Jean M. Hébert, a neuroscientist at Einstein.

“Is it the activation of the normal neural network that is causing the increase in these proteins and this behavior?” he said.

“We haven’t checked that yet.”

He also noted that the study, which was published Friday in the journal Science, potentially identified only a single source of hyperactivity, which is likely to have many causes.

“I wouldn’t start having hyperactive kids tested for their hearing,” he said.

Male sensitivity written in the genes

In human development, certain genes act as master switches, ensuring that we are born with similar attributes (one head, two lungs, 10 fingers) in nearly all circumstances. Such genes tend to be highly reliable and resistant to environmental factors.

But the gene responsible for activating male development is surprisingly unstable, leaving the pathway to male sexuality fraught with inconsistency, a study finds.

The SRY gene on the Y chromosome sets off the growth of male sex organs in human embryos (all of which start out essentially female).

To study the gene, researchers at Case Western Reserve University looked at families in which daughters inherited a Y chromosome, a rare occurrence in which SRY fails to fire, leaving a genetically male embryo to develop as a sterile female.

They found that SRY is highly vulnerable to environmental factors, allowing the slightest interruption to significantly alter male sexual development.

That leads to a wide divergence of testosterone-related male attributes (among them muscle mass, aggression and genitalia development) from one man to another, according to the study, which was published in The Proceedings of the National Academy of Sciences.

The variability probably serves an evolutionary purpose, said one of the authors, Dr. Michael Weiss.

“This tenuous switch is what underlies the variability of testosterone secretion in utero,” he said, producing men with a wide range of gender styles and capabilities that can help ensure a community’s survival.

New York Times Service