Researchers at the Yale School of Medicine have found a link between antisocial behavior and insufficient neuron development during adolescence.

A study by Yale Department of Psychiatry researchers found that mice with blocked neuron growth during their juvenile period exhibited altered social behavior later in life, unable to interact with other adults or to care for baby mice. Experts interviewed said that the findings, published Oct. 5 in The Journal of Neuroscience, may have potential applications in understanding schizophrenia and autism as well as the social deficits of children who undergo chemotherapy.

“This is the first time someone shows that changing neurogenesis during the juvenile period yields social defects,” Arie Kaffman, the assistant professor of psychiatry who led the research, said. Neurogenesis is the process by which new neurons are created in the brain.

Researchers placed transgenic mice, genetically modified to lack neurogenesis as adolescents, in enclosed boxes along with a control mouse, Kaffman said. To the surprise of the researchers who recorded their behavior, Kaffman said the transgenic mice ran away and hid in corners of the box every time the other mice approached them. In contrast, the control mice preferred to interact with the other mice in the box.

“If you put two mice together, they would normally like each other,” Lan Wei, a research scientist involved in the study, said. “But for our mice, the ones without neurogenesis in juvenile period, they keep away from other mice. They run away.”

According to Kaffman, to confirm that these results were really due to neurogenesis and not due to an impaired sense of smell, the researchers tested that ability in the mice. When the transgenic mice proved to have normal olfactory abilities, the researchers concluded that neurogenesis during the juvenile period is essential for socialization.

The researchers also tested mice with impaired adult neurogenesis but found that it did not cause antisocial behavior, Kaffman said. Only mice with impaired juvenile neurogenesis differed from the control mice in social behaivor.

“These results override previous belief that the social effects of impairment in adult and juvenile neurogenesis were the same,” Kaffman said.

The paper also confirmed previous findings that hindering neurogenesis in either adult or juvenile phases increases anxiety and decreased memory in adult female mice, demonstrating that age does not influence the role of neurons in some respects.

Wei said that these findings might provide insight on both the nature and symptoms of certain mental disorders, such as schizophrenia, which has been known to emerge during adolescence.

Michael J. Owens, professor of psychiatry and behavioral sciences at Emory University, said that the results might be important for child and adolescent cancer survivors who have received radiation or chemotherapy, because these treatments may decrease neurogenesis during important developmental periods. Just like the transgenic mice, survivors might show some antisocial behavior, he added.

Charles B. Nemeroff, a professor of psychiatry and behavioral studies at the University of Miami School of Medicine, also said that these results could have an impact on patients.

“We deal clinically with patients with early life trauma who have major difficulties with adult relationships,” Nemeroff said. “Part of this may well be the long term consequences of early life trauma on neurogenesis, particularly during this critical period in development.”

The next step for the researchers is to study the neural mechanisms of neurogenesis and to identify in which area of the brain it takes place, Kaffman said.

Michael J. Meaney of McGill University and Ronald S. Duman of Yale coauthored the paper with Kaffman and Wei.