Amnesia: 'Lost' Memories in Mice Retrieved with Light

Jun 01, 2015 03:45 PM EDT

Memories that have been "lost" as a result of amnesia have recently been retrieved in mice using light, according to a new study.

This process, known as optogenetics, gives scientists hope that effective treatments may one day be possible for retrograde amnesia in humans - which follows traumatic injury, stress, or diseases such as Alzheimer's.

It has long been debated whether memory loss is caused by damage to the neurons that store memories, or from a blockage of access to those memories.

"The majority of researchers have favored the storage theory, but we have shown in this paper that this majority theory is probably wrong," researcher Susumu Tonegawa from MIT said in a statement. "Amnesia is a problem of retrieval impairment."

When a memory is being formed, scientists speculate that a population of neurons is activated and undergoes lasting physical or chemical changes. This collection of neurons, known as "memory engram cells," can be triggered by a specific sight or smell, for example.

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By using optogenetics - in which proteins are added to neurons to allow them to be activated with light - Tonegawa and his colleagues showed for the first time that these neurons do indeed exist, in the region of the brain called the hippocampus.

However, it remained to be seen whether light could induce chemical changes in these neurons linked to memory consolidation. This involves "long-term potentiation" (LTP), or the strengthening of synapses that allow neurons to communicate with one another.

To find out if these chemical changes do indeed take place, the MIT team gave mice in the study a drug called anisomycin, which blocks protein synthesis within neurons and inhibits memory consolidation. But when they tried to reactivate the newly formed memory just a day later using an emotional trigger, they were unsuccessful.

"So even though the engram cells are there, without protein synthesis those cell synapses are not strengthened, and the memory is lost," Tonegawa explained.

On the other hand, when neurons involved in encoding the memory were stimulated with pulses of light, reactivating the protein synthesis, the animals were able to recall the memory in full.

"If you test memory recall with natural recall triggers in an anisomycin-treated animal, it will be amnesiac, you cannot induce memory recall," Tonegawa said. "But if you go directly to the putative engram-bearing cells and activate them with light, you can restore the memory, despite the fact that there has been no LTP."

These results suggest that mice that received the drug did not really "lose" their memory, but rather that access to the memory was simply blocked.

Further research is needed to confirm this mechanism, but it is a step in the right direction to better understanding and treating retrograde amnesia in human patients.

The findings are described in further detail in the journal Science.

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