Scientists reactivate lost memory of mice using light

Scientists have been able to reactivate the lost memory of mice using light, which helps to understand the biological mechanism of diseases such as amnesia and arouses the hope of new treatments, according to a study published in the journal Science.

This research sheds light on understanding the nature of amnesia, a controversial topic for neuroscience, says Susumu Tonegawa, a professor at the Massachusetts Institute of Technology (MIT) Learning and Memory Studies Center and director of the Riken Brain Science Institute at Japan, associated with MIT, who headed this work.

Researchers have been debating for years whether amnesia caused by head trauma, stress, or diseases such as Alzheimer's disease is due to damage to specific brain cells, which would make it impossible to regain memory, or if access to these memories is the result. That represents a problem.

"Most scientists prefer the theory of destruction of information storage, but this research shows that this is probably wrong, " says Professor Tonegawa, Nobel Prize winner in medicine in 1987. "Amnesia is a problem of memory retrieval, " he says. .

Scientists assumed that there was in the brain a network of neurons that, activated during the formation of a memory, cause physical or chemical changes called engrams.

The hippocampus of the brain

According to scientists, if these clusters of engram neurons are reactivated by an image, an odor or a taste, all recorded memory should return. To demonstrate the existence of memory memory cells in the hippocampus of the brain, this group of scientists used mouse optogenetics, which is to add proteins to neurons to enable them to be activated by light.

Until now, it had not been possible to demonstrate that these engram neurons were chemically modified by a process called memory consolidation.

One of the key changes is to reinforce synapses, structures that allow messages to be transmitted between neurons from learning and experience.

These scientists also tried to see what would happen if this synapse consolidation would not happen. They gave a group of rodents a chemical, anisomycin, which blocks protein synthesis in neurons immediately after a new memory is formed, preventing this consolidation.

A group of animals were placed in a cage called A, where they suffered electric shock to their paws. Later, when they wanted to put them back in the cage, the animals showed fear, indicating that they remembered a traumatic experience. On the contrary, another set of rodents, which had no memory of it, did not react.

Then the scientists reactivated the process of synapse consolidation by impulses in amnesia rats, which fully recovered the memory of the electrical discharge. Even when placed in another cage, they were paralyzed by fear.

The study allowed us to differentiate memory storage mechanisms from those that allow it to be formed and retrieved, emphasizes Thomas Ryan, a researcher at MIT, the main co-author of this research. For Professor Tonegawa, this shows that in some forms of amnesia, the memory may not have been erased, but is simply "inaccessible."

According to him, "these works shed surprising light on the nature of memory and will stimulate future research on memory biology and its clinical restructuring."

By Jean-Louis Santini - Washington

Via InSummary.