Newly Identified Anatomical Circuit In The Brain Explains Clinical Depression
Many cases of depression are treatment-resistant and those with the disease can spend much of their lives very sad and generally unresponsive to anything positive that might arise in their lives.
The newest experimental treatment for these types of depression has been deep brain stimulation (DBS), a treatment that involves the implantation of a brain pacemaker inserted in the chest that sends electrical signals to brain tissue. DBS has also been used to control epilepsy, Parkinson's disease, and other neurological disorders, although different systems in the brain may be targeted.
Today, in the journal Nature, researchers from the Brookhaven National Laboratory, Cold Spring Harbor Laboratory, and the University of California, San Diego reveal their discovery of a specific region of the brain that is affected during 'chronic,' or untreatable depression. The region is called the lateral habenula, and the activity produced by this region is cellular.
Cells in the lateral habenula are activated by unpleasant events, including punishment and disappointment. The scientists used two animal models - one of 'learned helplessness' and a control group. (Learned helplessness imitates the brain activity of depression.) They found what they expected; hyperactivity of the lateral habenula in the helpless rodents and no activity in the control group. But they also found that dopamine, the reward system of the brain, was shut off in the brains of rats that had depression, or learned helplessness.
Scientists then attempted DBS, placing stimulating electrodes in the lateral habenula area of the depressed rats, and then measuring the effects on the reward center of the brain. They found that stimulating the lateral habenula area of the brains "can acutely reverse helpless behavior in rats."
"It's very likely that this beneficial effect was mediated by a suppression of excitatory nerve cells leading to the brain's reward system, as we observed in the cellular studies," said Fritz Henn, a neurobiologist and psychiatrist at Brookhaven and Cold Spring Harbor laboratories and a co-investigator on the research.
"Our study provides a cellular mechanism that may explain the hyperactivity of lateral habenula nerve cells observed in depressed humans and animal models of depression, as well as why 'silencing' these circuits, whether surgically or pharmacologically, can reduce depression-like symptoms in animals," Henn said.