Ed Yong, in a post on his blog Not Exactly Rocket Science (now at Discover, but moving next week to National Geographic), does a nice job of sorting out what's going on in a pair of studies that seem to show contradictory findings about depression and certain neurons in a particular region of the brain.
In one study, a "depressed" mouse–one that's been exposed to chronic stress and now seems timid and less likely to seek out rewards–recovered almost instantly when cells in its ventral tegmental area, or VTA, were activated. (This was done by modifying the mouse so that a flash of light would activate only those cells–a technique called optogenetics.)
A potential new treatment for depression? Not so fast. In another study, researchers found that activating cells in that area using the same technique made mice that had been exposed to stress more likely to be susceptible to depression.
Yong sets up this apparent contradiction and then neatly explains what appears to be happening. The mice could be reacting differently to different kinds of stress-becoming more susceptible when exposed to shorter, more intense stress than when exposed to chronic stress. It's the difference between, say, getting mugged, or facing job insecurity. The results "underscore the complicated nature of depression," Yong writes.
He could have stopped there, but he continues by noting that the VTA is "a hub for neurons that secrete dopamine," and that both studies show the importance of dopamine in depression. They also show the importance of the circuit that involves not only the VTA but its connections to the nucleus accumbens, or NA. And both studies show that manipulation of this circuit can affect depression in minutes.
Yong makes this circuitry clearer than I am. And while his story reflects excitement about the findings, it also carefully notes that we should not expect a new treatment soon–precisely the kind of balance that's nice to see in reporting groundbreaking findings such as these.
-Paul Raeburn
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