Scientists from Scripps Research have discovered a memory gating system that employs dopamine to direct transient forgetting. Their findings were published in Nature Communications.

The study adds a new pin to scientists' evolving map of how learning, memory and active forgetting work, says lead researcher Ron Davis. "This is the first time a mechanism has been discovered for transient memory lapse," Davis says. "There's every reason to believe, because of conservation biology, that a similar mechanism exists in humans as well."

To understand the mechanisms behind transient forgetting, the team worked in the common fruit fly, a model favored by neurobiologists for decades due to its relatively simple brain structure, ease of study and translatability to more complex animals. The team put their flies through a series of training exercises, teaching them to associate an odor with an unpleasant foot shock. They then watched as several interfering stimuli, such as a blue light or a puff of air, distracted the flies so they forgot the odor's negative association, temporarily. Interestingly, stronger stimulation led to longer lasting periods of forgetting.

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Additional biochemical studies revealed a single pair of dopamine-releasing neurons in the flies, called PPL1-α2α'2, which directed the transient forgetting. Dopamine sent from other neurons didn't have the same effect. The neurons activated dopamine receptors called DAMB on axons extending from neurons in the memory-processing center of the fruit fly brain.

"We now know that there is a specific receptor in the memory center that receives the transient forgetting signal from dopamine. But we don't yet know what happens downstream. What does that receptor do to the physiology of the neuron that temporarily blocks memory retrieval? That's the major next goal, to understand how this block in retrieval occurs through the activation of this dopamine receptor," Davis says. "We are just at the very beginning of understanding how the brain causes transient forgetting."