WASHINGTON, June 4 (Xinhua) -- A new study published on Monday in the journal Proceedings of the National Academy of Sciences has shown how two proteins spring into action to ensure that a memory is encoded within minutes in mice.
Neurogranin and Fragile X Mental Retardation protein (FMRP) that could team up to make memory are also present in humans. FMRP gets its name because it is central to the genetic, autism-like condition Fragile X syndrome, and neurogranin is linked to schizophrenia and intellectual disability.
The protein making associated with new memory formation occurs at sites called synapses where neurons connect in circuits with other neurons, according to the study. This can be driven by neural activity triggered by specific events, such as encountering a novel place.
The new study also provided new hints about how problems involving these two proteins in other parts of the brain, such as the frontal cortex, could undermine cognition in those diseases.
Xu Weifeng, assistant professor in the Department of Brain and Cognitive Sciences at Massachusetts Institute of Technology (MIT) and Kendrick Jones at MIT's Picower Institute for Learning and Memory conducted experiments in mice in a memory-making region called the hippocampus.
Xu's team used a drug to temporarily interrupt neural protein-making at four different time points when introducing mice to a new space.
Based on results from testing the memories of the mice the next day, the researchers found that if they administered the drug 30 minutes before or exactly at the moment of introducing mice to the new space, they could prevent memory formation, but administering the drug immediately after or shortly after the context exposure had no effect on memory formation.
It revealed that the new protein synthesis required for context memory formation has a rapid onset, and is transient, Xu said.
The scientists also found neurogranin showed a marked increase of messenger RNA in the protein-making machinery, or ribosomes, of the mice who were exposed to a new place.
By specifically blocking the neurogranin's activity in mice, the memory formation has been prevented, according to the study.
Then the researchers probed the nature of neurogranin's translational regulation, and identified FMRP as an interaction partner of the neurogranin messenger RNA.
By knocking out the FMRP gene they could observe that without it, mice didn't make extra neurogranin when exposed to new places and didn't form a memory, according to the study.
