Boosting the activity of newly-created neurons mimicked the effect of antidepressant medication in animal models, according to a recent Northwestern Medicine study published in Nature Communications.
The discovery may point to a new understanding of how to treat depression, said Dr. John Kessler, the Ken and Ruth Davee Professor of Stem Cell Biology and senior author of the study.
The effects of depression are well-documented, but its causal mechanisms are still up for debate, according to Dr. Kessler. Most scientists agree that chemical imbalances in the brain are a primary factor, but the source of those imbalances remains murky.
Some evidence implicates changes in the rate of neurogenesis, the process by which new neurons are created from specialized neural stem cells in the hippocampus, Dr. Kessler explained.
Dr. Kessler, along with Dr. Elif Tunc-Ozcan, a postdoctoral fellow and lead author of the study, set out to test if neurogenesis could directly alter depression symptoms. The investigators genetically altered mice so neurons created in adulthood had a kill switch, a receptor that could be activated by a drug.
When neurogenesis was silenced, the scientists found anti-depressant drugs no longer worked, speaking to neurogenesis’ importance in modulating depression-like symptoms. Next, in a similar but opposite experiment, the investigators inserted an excitatory receptor into the newly created neurons.
When they activated this receptor, it was as if the mice were treated with Prozac, according to Dr. Tunc-Ozcan. This was surprising because they hadn’t increased neuron production, just boosted neuronal activity.Friday Letter Submission, Publish on September 27