SCIENCE FILE : Stressed-out kid to depressed adult? : Early stress can result in higher risks of neurological and behavioral problems, a new study finds.
Growing up in a stressful environment isn’t conducive to becoming a well-adjusted adult. Studies have shown that people who faced constant stress during childhood have an increased risk of being depressed later.
How are the two related? A study published this week by the journal Nature Neuroscience may have found a link. It reports that stress at a young age permanently alters the activity of a key gene in the brain, resulting in a lifetime of elevated levels of a hormone that contributes to depression.
To figure this out, a team of German researchers stressed baby mice by separating them from their mothers for three hours a day during their first 10 days of life. Other mice were kept with their mothers continuously, to serve as controls.
The animals’ blood was tested when they were 6 weeks, 3 months and 1 year old. The mice that had been removed from their mothers’ nests had higher levels of the stress-related hormone corticosterone circulating in their blood than their counterparts, the researchers found.
When the animals were subjected to stressful situations, mice who’d been traumatized produced more corticosterone in response to that stress than did the controls.
The researchers, from the Max Planck Institute of Psychiatry in Munich, Germany, found behavioral deficits in the high-stress mice too. They were more likely to freeze up in forced swim tests, and had memory problems with certain tasks.
The researchers traced these problems to chemical changes in a gene responsible for making the hormone arginine vasopressin. These changes prompted the mice to make too much of the hormone. Arginine vasopressin influences a variety of traits, including mood.
To confirm that arginine vasopressin was responsible for the stress, the researchers gave the stressed-out mice a drug that blocked the hormone’s effects in the brain. The mice then produced normal levels of corticosterone.
“Our results suggest that adverse events in early life can leave persistent . . . marks on specific genes that may prime susceptibility to neuroendocrine and behavioral dysfunction,” the authors concluded.
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