asurable stimuli, drinking significantly less of a sugar-water solution than normal mice.
The depression-like behaviors closely corresponded to physiological changes. Four- and six-month-old engineered mice had significantly higher blood levels of glucocorticoid than normal mice. While normal mice suppressed their production of glucocorticoid when given a synthetic substitute hormone, the engineered mice showed no change in glucocorticoid levels, demonstrating an impairment in their ability to properly regulate their stress response.
The abnormal regulation of glucocorticoid in the engineered mice indicates that glucocorticoid receptors in the cortex and hippocampus—forebrain regions associated with higher thought, memory, and emotion—regulate adrenal hormone levels. This regulatory role for forebrain cells has not been previously proven.
“Our findings in mice lacking glucocorticoid receptors suggest that some people may have a genetic makeup that reacts to stressful experiences by turning down the activity of the glucocorticoid receptor gene,” Muglia says. “This may initiate a process leading to depression.”
Using the engineered mice, the researchers next will seek genes that interact with glucocorticoid receptors and investigate the mechanism of action of antidepressant drugs. The projects will provide a fuller understanding of the underlying causes of depression and could lead to the development of new, more effective antidepressants, according to Muglia.
Boyle MP, Brewer JA, Funatsu M, Wozniak DF, Tsien JZ, Izumi Y, Muglia LJ. The acquired deficit of the forebrain glucocorticoid receptor produces depression-like changes in adrenal axis regulation and behavior. Proceedings of the National Academy of Sciences, January 2005.
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