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Scientists Retrieve Lost Memories Using Light To Activate Proteins on Neurones

What happens to lost memories, and where do they go? Can they be retrieved from their hiding place? A new study published in Science has provided new insight into the nature of memories by finding and bringing back lost memories using light.

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The scientists behind the study wanted to determine whether amnesia causes memories to be lost from a group of brain cells to another, or whether, the storage of the memories is “faulty”.

“Brain researchers have been divided for decades on whether amnesia is caused by an impairment in the storage of a memory, or in its recall,” says lead researcher Susumu Tonegawa, from the RIKEN-MIT Center for Neural Circuit Genetics, in a statement.

The researchers favour the latter.

“The majority of researchers have favored the storage theory, but we have shown in this paper that this majority theory is probably wrong. Amnesia is a problem of retrieval impairment,” he explains.

The team made mice to succumb to amnesia by causing them to associate a mild foot shock given to them with an environment called chamber A such that when the animals would enter the latter, they would demonstrate a characteristic “freezing” behaviour. Those neurones that were activated when this specific memory was formed were identified and labelled. Then, one group of the mice was made to forget this memory.

To cause amnesia, the scientists administrated a substance called anisomycin to inhibit protein synthesis, thereby decreasing the length of synapses that are important to memory encoding. This group of mice, suffering from amnesia, did not freeze when entering chamber A, while the control group (the mice without anisomycin) did.

Thereafter, the researchers sought to find out whether this lost memory could be brought back. They made use of optogenetic techniques: using light, they activated proteins that were added to the neurones. The scientists were ultimately successful in activating the specific neurones linked with the memory of the mild foot shock upon entering chamber A. Both groups of mice were then made to enter a new environment, chamber B. They all “froze” when the cells associated with the shock memory were activated.

According to the researchers, different brain processes govern the storage and recalling of memories. This is explained in terms of “memory consolidation”, a term meaning that groups of neurones are subject to a durable chemical change. The researchers note that they observed a specific change known as “long-term potentiation” whereby synapses grew stronger with learning and experience.

The anisomycin rendered the synapses less strong by decreasing their length.
When using an emotional trigger to retrieve the memory of the mice, nothing happened: the synapses were not made stronger because the required protein synthesis did not happen, and the memory was therefore lost. The opposite happened when protein synthesis occurred: the memory was retrieved.

“Our conclusion is that in retrograde amnesia, past memories may not be erased, but could simply be lost and inaccessible for recall. These findings provide striking insight into the fleeting nature of memories, and will stimulate future research on the biology of memory and its clinical restoration,” says Tonegawa.

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