A team of researchers at Stanford have successfully induced and relieved depression-like deficiencies in both pleasure and motivation in mice by controlling a region of the brain known as the ventral tegmental area. That part of the brain is a source of dopamine and a central player in the brain’s internal motivation and reward systems.
This is a significant advance in our understanding of the biological underpinnings of depression and related behaviors, with promising implications for future research
More details on the study are offered in a release:
[Researchers were] able to both induce and relieve multiple depression-like symptoms in laboratory mice by genetically modifying the dopamine neurons in the VTA to be sensitive to light. Using fiber optic cables inserted in rodents’ brains, they could then instantaneously produce and inhibit the depression-like symptoms by turning the light on and off. This research technique, developed by Deisseroth at Stanford in 2005, is known as optogenetics.
The team examined mice in a depressed-like, low-motivation state induced by mild stressors whose VTA neurons had been optogenetically modified. “When given light stimulation to the VTA dopamine neurons, these mice showed a robust increase in escape-related behavior. They immediately tried harder to get out of challenging situations — reversing back to normal levels of effort from the depressed-like state they were in,” explained Deisseroth.
Stanford bioengineer and senior author of the study Karl Deisseroth, MD, PhD, commented on the significance of the findings, saying, “These results directly implicated a single class of neuron in a single brain region — ventral tegmental dopamine neurons — in both producing and relieving very different depression-related symptoms, addressing a mystery in disease pathophysiology.”
While the results (subscription required) are notable, Deisseroth cautioned that depression and other mental illnesses are complex, multidimensional conditions that vary among patients. But, he said,
…the VTA dopamine circuitry we studied is very similar in both rodents and humans. And we have shown that the neurons in this circuit specifically cause, correct and encode diverse symptoms of depression. This is a significant advance in our understanding of the biological underpinnings of depression and related behaviors, with promising implications for future research.