You get up to go to another room, but once you’re there you forget why you came to the room in the first place. Has this ever happened to you? Researchers at Scripps Research report they have uncovered the culprit behind transient forgetting, the temporary lapse of memory that spontaneously returns.
Their findings are published in the journal Nature in a paper titled, “Dopamine-based mechanism for transient forgetting.”
“Active forgetting is an essential component of the memory management system of the brain,” the researchers wrote. “Forgetting can be permanent, in which prior memory is lost completely, or transient, in which memory exists in a temporary state of impaired retrieval. Temporary blocks on memory seem to be universal, and can disrupt an individual’s plans, social interactions, and ability to make rapid, flexible, and appropriate choices. However, the neurobiological mechanisms that cause transient forgetting are unknown. Here we identify a single dopamine neuron in Drosophila that mediates the memory suppression that results in transient forgetting.”
“This is the first time a mechanism has been discovered for transient memory lapse,” stated Scripps Research neuroscience professor Ron Davis, PhD. “There’s every reason to believe, because of conservation biology, that a similar mechanism exists in humans as well.”
The researchers worked in the common fruit fly, a model favored by neurobiologists for decades due to its relatively simple brain structure. The flies were put through a series of training exercises, teaching them to associate an odor with an unpleasant foot shock. The researchers then observed 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. They also noted that stronger stimulation led to longer lasting periods of forgetting.
Additional biochemical studies revealed a single pair of dopamine-releasing neurons in the flies, called PPL1-α2α’2, which directed the transient forgetting.
Activation of the transient forgetting circuit did not erase the flies’ long-term memory recall, suggesting that transient forgetting doesn’t affect permanent, consolidated memory traces, or engrams, that are acquired over time, Davis said.
The flies’ memory performance was restored after the transient forgetting period lifted, stated John Martin Sabandal, a Scripps Research graduate student, who worked with staff scientist Jacob Berry, PhD, at the team’s lab in Jupiter, Florida.
“Could we perform better if certain memories are suppressed over others—could we learn or adapt to situations better? Nobody knows. Those are the type of questions that will be explored in the future,” Sabandal said. “We found, provisionally, there is a potential memory reserve that is just unable to be expressed at a particular moment.”
Previously, in 2012, Davis’ group found a mechanism directing permanent forgetting, finding it is an ongoing, active process needed for healthy brain function.
“You can imagine that we have thousands of memories that occur every day in our lifetime, and the brain does not have the capability of remembering, or encoding, all of those memories. So there is a need to erase those memories that are irrelevant to our existence and our daily lives,” Davis added.
Their findings are just the tip of the iceberg. The researchers look forward to learning more about the receptor and understanding how the brain causes transient forgetting.
“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 said. “We are just at the very beginning of understanding how the brain causes transient forgetting.”