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Adolescent Stress Can Change Brain During Adulthood

Adolescent Stress Can Change Brain During Adulthood

FOR IMMEDIATE RELEASE:
November 08, 2003

CONTACT:
Cindy Lepore, Adriana Bobinchock
617/855-2110
leporec@mclean.harvard.edu

Belmont, MA - Studies by Susan Andersen, PhD, of McLean Hospital and colleagues show that stressful events experienced during adolescence can lead to enduring changes in brain structure in adulthood. This work, being presented Nov. 8 at the Society for Neuroscience's Annual Meeting in New Orleans, is the first to demonstrate that exposure to a significant stress during adolescence can impact neuronal connections in the adult brain.

The researchers found that adult rats exposed to a social stress during adolescence (ages approximating 13 to 15 years in humans) showed a significant decrease in a specific protein found in the hippocampus, a brain region important for learning and memory. In fact, the loss of this protein, synaptophysin, is at least as great as that occurring in animals exposed to more severe stressors at a younger age, suggesting that adolescents may be more vulnerable to the effects of stress than younger animals.

Under typical conditions, synaptophysin, which is often used as an index of the number of neuronal connections, or synapses, reaches a peak during young adulthood (approximately ages 18 to 20), with the rise occurring primarily during adolescence. The team tested whether a social stress during this key developmental period might alter this pattern. A control group of rats was housed with their peers, and an experimental group of rats was housed individually during adolescence; individual housing in normally social animals such as rats is a stressful experience. The brains of both groups were then examined during young adulthood. The team found that rats exposed to the social stressor did not show the normal increase in synaptophysin during this period. These data suggest that social stress during adolescence causes either a loss of synapses or a decrease in the synaptophysin protein.

The researchers then compared the loss of synaptophysin in rats that were stressed during adolescence with rats that experienced significant stress during ages comparable to childhood. The stressor used for this age group was repeated maternal separation (RMS). The scientists found no significant difference in synaptic density between rats that had social stress during adolescence or rats that had early RMS. However, the density of synapses in the hippocampus of both groups was reduced significantly when compared with control rats.

These findings are the first to demonstrate that exposure to a significant stress during adolescence can have enduring consequences on the connections formed in the hippocampus in adulthood. These data may suggest why early traumatic stress, such as physical or sexual abuse or neglect, is associated with a decrease in the size of the hippocampus in adulthood.

"These pre-clinical data suggest that stress experienced early in life alters the normal developmental trajectory of the hippocampus, but that these changes are not apparent until later in life," said Andersen.

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