New neurons are associated with improvement of depression in mice.

Investigators at the Stanford University School of Medicine believe that they have found one unifying principle that could explain how a range of causes and treatments for depression converge. They discovered that in rats the differing mechanisms of depression and its treatment  appear to funnel through a single brain circuit. Changes in how the electrical signals spread through the circuit appear to be the cause of depression-related behavior, according to their study.

Reasoning that the brain is essentially a complex electrical circuit, the team set out to test the theory of whether a circuitry malfunction could be at the root of depression. To explore the idea in a precise, quantitative way, they needed to develop a visualization tool that was faster and sharper than brain imaging systems currently available.

The researchers developed a technique called voltage-sensitive dye imaging. This technique allows intact brain circuits to be viewed in real time, enabling the researchers to watch living neurons in action across entire brain networks.

The team used slices of rat brain, which remain active for many hours, that came from parts of the hippocampus. They also tested slices from rats treated with the antidepressant medications fluoxetine and imipramine.

The scientists found an alteration in electrical activity flow through the brain that could be corrected by human antidepressants. The extent that the signal spread through the brain sample was diminished in the depressed rats.

While searching for the cellular basis of these changes in circuitry, they found that the growth of new neurons could account for the behavioral improvements seen from treatment as well as the circuitry changes. However, they discovered that fewer new neurons in that region did not equal depression.

Their findings were published in the July 6 issue of Science Express.

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