When a long-term memory is formed, some brain cells experience very rapid electrical activity so strong that it "cuts" their DNA.
An inflammatory response then begins to set in, repairing that damage and helping to boost memory, according to research conducted in mousea.
The findings, which were published March 27 in Nature, are "exciting," says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge, who was not involved in the work.
They contribute to the image that creating memories is a very "risky business," says Li-Huei Tsai.
Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the cycle of DNA damage and repair gives us an explanation for how memories can form and last.
It also gives us a tantalizing hypothesis: This cycle may be defective in people with neurodegenerative diseases like Alzheimer's, causing errors to accumulate in a neuron's DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City.
To better understand the role these DNA "breaks" play in long-term memory formation, Radulovic and her colleagues trained mice to associate a small electric shock with a new environment, so that when the animals are put back into that environment, they "remember" their not-so-pleasant experience and show signs of fear, such as freezing in place.
The researchers then looked at gene activity in the neurons in a region of the brain key for memory – the hippocampus.
So they found that certain genes responsible for inflammation were active in a set of neurons four days after the experiment. Three weeks after the experiment, the same genes were much less active.
