Genetics Could Keep Mickey and Minnie Together

Scientists turn promiscuous male mice into monogamous mates

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HealthDay Reporter

WEDNESDAY, June 16, 2004 (HealthDayNews) -- Could a single gene explain why some men are life-long Lotharios while others are satisfied with a single soulmate?

In genetic experiments with mice, researchers have been able to turn promiscuous males into monogamous mates.

And while some experts were skeptical that the experiment could have any implication for humans, they did say the research demonstrated that some human social behaviors are rooted in biology.

Emory University researchers found that by transferring a single gene -- called the vasopressin receptor -- from the brains of monogamous male prairie mice into the brains of promiscuous male meadow mice, the meadow mice became monogamous, too.

"Variation in a single gene can have an impact on complex social behavior," said lead researcher Larry J. Young, an assistant professor in the department of psychiatry and behavioral sciences at the university's School of Medicine in Atlanta.

"And this gene, the vasopressin receptor, is involved in pair bonding," he added.

To find out how the gene affected behavior, Young's team studied two types of mice -- the very social prairie mice and the not-so-social meadow mice.

The difference between these mice is the location of the vasopressin receptor gene in their brain, Young said.

"There is a part of the brain that is involved in drug addiction that in monogamous mice has lots of vasopressin receptors. In the non-monogamous mice, there are none," he said.

The researchers took vasopressin receptor genes from the monogamous mice and put them into the same part of the brain in the non-monogamous mice, according to the report on the June 17 online issue of the journal Nature.

"We found that those animals now bonded with their mate, when normally this species would not do that," Young said. "This suggests that a single gene can have a profound affect on social behavior."

"This gene variation that we see in these two species of mice might be similar to variations that we see in humans," he added. "It may explain why some humans behave differently than others, particularly when you talk about some diseases such as autism."

Autism is a disruption in social behavior, and it may be that this gene is involved in the disorder, Young noted.

The gene could also explain some of the natural variations in personality when it comes to social behavior.

"This gene could influence whether you are outgoing or shy, or even how you form attachments and relationships with other people," Young said.

Dr. David L. Katz, an associate clinical professor at Yale University's Schools of Public Health and Medicine, said, "This finding demonstrates a powerful and simple genetic basis for social bonds and monogamy, but will almost certainly fail to translate directly into humans."

However, he noted, the finding is important because it shows how some tendencies that might be considered purely behavioral may, in fact, be tied to genetics.

"We, like other species, are creatures with specific traits and tendencies encoded in our genes. And that has implications for everything from the foods we like to eat and our susceptibility to weight gain, to our social, romantic and sexual inclinations," Katz said.

This research is also humbling, he added, because it points out the hidden ways in which humans may not fully be their own masters.

"But values, social conventions and love are powerful attributes in humans, lacking, so far as we know, in mice. We should be sobered by knowledge of our biological predispositions. Unlike most other creatures, we need not be bound by them," Katz said.

More information

The Human Genome Project can tell you more about genes and behavior.

SOURCES: Larry J. Young, Ph.D., assistant professor, department of psychiatry and behavioral sciences, Emory University School of Medicine, Atlanta; David L. Katz, M.D., M.P.H., associate clinical professor, Yale University Schools of Public Health and Medicine, director, Yale Prevention Research Center, New Haven, Conn.; June 16, 2004, online edition, Nature

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