One of the interesting results of Luscher's new research is that some antidepressant drugs completely reverse the behavioral and hormonal symptoms of depression in the GABA-A-receptor-deficient mice, bringing their behavior to the level of normal, "wild-type" mice. At the same time, the normal mice had almost no reaction to the drugs. "This result is expected of a mouse model that mimics depression because normal people do not seem to gain anything from taking antidepressants," Luscher explained. These experiments show that this strain of genetically defective mice is a useful animal model for laboratory studies that could be useful for understanding human depression.
One of the major gaps of knowledge about depression in humans is that scientists do not know why some antidepressant drugs fail to help about 30 percent of depressed patients. Because doctors don't have a way of knowing which drug has the best chance of working for a particular patient, they resort to trying one after another hoping to find one that will work. This problem is compounded by the fact that it can take weeks before the drugs show any measurable benefit.
Luscher's team tested two kinds of antidepressant drugs in the mice and found that one of the drugs reduced symptoms of anxiety, but not of depression, whereas the other drug reduced both anxiety and depression symptoms. "The one that did not normalize depression-related behaviors is fluoxetine -- the generic name for Prozac -- which works on the neurotransmitter serotonin," Luscher said. The drug that reduced both depression and anx
|Contact: Barbara K. Kennedy|