The Huck Institutes of the Life Sciences

Genetically defective mice shed new light on treating depression

Researchers led by Dr. Bernhard Luscher have characterized a new mouse model of depression that points to a new cause of Major Depressive Disorder in humans. The mice suffer from a genetic deficiency in GABA-A-receptors, and they exhibit hormonal and pharmacological properties indicative of a form of depression known as Melancholic Depression.

People with Melancholic Depression do not respond well to the popular anti-depressant drug Prozac, which acts on the neurotransmitter serotonin, but may be one step closer to relief thanks to these mice. The mouse model demonstrates depression-related symptoms comparable to those of people suffering from drug-resistant forms of melancholic depression: they are less likely to explore new environments, show signs of behavioral despair, and they exhibit diminished pleasure seeking behavior. They also show increased serum levels of the hormone corticosterone, or cortisol as it is known in humans, which is typical of melancholic depression. Dr. Luscher's team was able to show that fluoxetine (Prozac) reversed only some of these symptoms, whereas another antidepressant, desipramine, that tends to be more effective in melancholic depression, completely normalized all the symptoms of the mice. These studies suggest that patients suffering from Melancholic Depression may suffer from a deficit in GABAergic neurotransmission.

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