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To understand how neurogenesis—the process of creating new brain cells— works, Gould’s lab studies the effect of two separate variables: stress and enriched environments. Chronic stress, predictably enough, decreases neurogenesis. As Christian Mirescu, one of Gould’s post-docs, put it, “When a brain is worried, it’s just thinking about survival. It isn’t interested in investing in new cells for the future.”

On the other hand, enriched animal environments—enclosures that simulate the complexity of a natural habitat—lead to dramatic increases in both neurogenesis and the density of neuronal dendrites, the branches that connect one neuron to another. Complex surroundings create a complex brain.

The subject of stress has been the single continuous thread running through Gould’s research career. From the brain’s perspective, stress is primarily signaled by an increase in the bloodstream of a class of steroid called glucocorticoids, which put the body on a heightened state of alert. But glucocorticoids can have one nasty side-effect: They are toxic for the brain. When stress becomes chronic, neurons stop investing in themselves. Neurogenesis ceases. Dendrites disappear. The hippocampus, a part of the brain essential for learning and memory, begins withering away.

Gould’s insight was that understanding how stress damages the brain could illuminate the general mechanisms—especially neurogenesis—by which the brain is affected by its environ-mental conditions.

“Poverty is stress,” she says, with more than a little passion in her voice. “One thing that always strikes me is that when you ask Americans why the poor are poor, they always say it’s because they don’t work hard enough, or don’t want to do better. They act like poverty is a character issue.”

Gould’s work implies that the symptoms of poverty are not simply states of mind; they actually warp the mind. Because neurons are designed to reflect their circumstances, not to rise above them, the monotonous stress of living in a slum literally limits the brain.

When Duman began studying the molecular basis of antidepressants back in the early 90s, the first thing he realized was that the serotonin hypothesis made no sense. A competing theory, which was supposed to explain the Prozaz lag, was that antidepressants increase the number of serotonin receptors. However, that theory was also disproved. “It quickly became clear that serotonin wasn’t the whole story,” Duman says. “Our working hypothesis at the time just wasn’t right.”

But if missing serotonin isn’t the underlying cause of depression, then how do antidepressants work? As millions will attest, Prozac does do something. Duman’s insight, which he began to test gradually, was that a range of antidepressants trigger a molecular pathway that has little, if anything, to do with serotonin. Instead, this chemical cascade leads to an increase in the production of a class of proteins known as trophic factors. Trophic factors make neurons grow. What water and sun do for trees, trophic factors do for brain cells. Depression was like an extended drought: It deprived neurons of the sustenance they need.

Though Gould’s lab has thoroughly demonstrated the long-term consequences of deprivation and stress, the brain, like skin, can heal itself, as Gould is now beginning to document, finding hopeful antidotes to neurogenesis-inhibiting injuries. “My hunch is that a lot of these abnormalities [caused by stress] can be fixed in adulthood,” she says. “I think that there’s a lot of evidence for the resiliency of the brain.”

On a cellular level, the scars of stress can literally be healed by learning new things.