While forgetting is normal, exactly how we forget — the brain processes guiding the process — has been, until now, poorly understood.
But now scientists from the Florida campus of The Scripps Research Institute say they have pinpointed a mechanism that is as essential for forming memories as it is for forgetting those memories.
“This study focuses on the molecular biology of active forgetting,” said Ron Davis, chair of the Scripps Research Department of Neuroscience who led the project. “Until now, the basic thought has been that forgetting is mostly a passive process. Our findings make clear that forgetting is an active process that is probably regulated.”
Davis and his colleagues studied fruit flies, which are often used for studying memory. The flies were put in situations where they learned that certain smells were associated with either a positive reinforcement like food or a negative one, such as a mild electric shock. The scientists then observed changes in the flies’ brains as they remembered or forgot the new information.
The results showed that a pair of dopamine receptors actively regulate the acquisition of memories and the forgetting of these memories.
The results suggests that when a new memory is formed, there also exists an active, dopamine-based forgetting mechanism — ongoing dopamine neuron activity — that begins to erase those memories unless some importance is attached to them.
The scientists found that specific neurons in the brain release dopamine to two different receptors known as dDA1 and DAMB, part of a densely packed network of neurons vital for memory and learning in insects. The study found the dDA1 receptor is responsible for memory acquisition, while DAMB is required for forgetting.
When dopamine neurons begin the signaling process, the dDA1 receptor becomes overstimulated and begins to form memories. Once that memory is acquired, however, these same dopamine neurons continue signaling. Except this time, the signal goes through the DAMB receptor, which triggers forgetting of those recently acquired, but not yet consolidated, memories.
Jacob Berry, a graduate student in the Davis lab who led the experiments, showed that inhibiting the dopamine signaling after learning enhanced the flies’ memory. Boosting the activity of those same neurons after learning erased memory. The researchers also found that a mutation in the dDA1 receptor produced flies unable to learn, while a mutation in the other, DAMB, blocked forgetting.
The study sheds light on a number of issues, including savant syndrome, Davis said.
“Savants have a high capacity for memory in some specialized areas,” he said. “But maybe it isn’t memory that gives them this capacity, maybe they have a bad forgetting mechanism. This also might be a strategy for developing drugs to promote cognition and memory — what about drugs that inhibit forgetting as cognitive enhancers?”
The study, supported by the National Institutes of Health, appears in the May 10, 2012 issue of the journal Neuron.
Source: The Scripps Research Institute