HANGZHOU, Feb. 13 (Xinhua) -- Chinese researchers have found that immune cells in the brain can eat up memories, revealing mechanisms behind people's ability to forget.
Previous studies found that a group of neurons called engram cells are activated during the process of learning, and synapses, large webs of precise connections linking engram cells, play a big role in memory storage. When people recall specific memories, engram cells are reactivated.
In the new study, researchers from Zhejiang University gave an unpleasant memory to mice. The mice got electric shocks when they got in a special cage. Five days after the shocks, the mice would still freeze in fear when they were placed in the cage.
But 35 days later, the mice began to forget and froze less often in the cage. The analysis showed fewer engram cells were reactivated.
The researchers then removed microglia in some mice' brains. Microglia are a type of neuroglia located throughout the brain and spinal cord, accounting for 10 to 15 percent of all cells found within the brain. They primarily act as immune cells.
They reported on the journal Science that mice with fewer microglia held on to the scary memory and their freezing time in the cage was double those with a normal number of microglia.
They also used drugs to block certain pathways, making microglia in the mice brain unable to chew up synapses. Those mice also held on to the scary memories, freezing more in the cage.
According to the researchers, microglia are like demolition workers of the brain, tearing down and remove targets they perceive as unnecessary, undesirable or damaging to the living neurons.
It could explain why review can improve memories in learning. Without review, synapses are like desolated bridges connecting engram cells and could be demolished and cleaned up by microglia.
They said the study lays the groundwork for future studies in long-term memory consolidation and unpleasant memory elimination. They also expect to have a clearer understanding of memory impairment and memory loss caused by diseases in future studies.