"For example, if a person were reading a page of a textbook, it might take several times to memorize it," Costa-Mattioli said. "A human equivalent of these mice would get the information right away."
The mutant mice also performed better than normal mice in a "fear-conditioning" test. In that test, animals are put into a cage followed by a mild foot shock or are exposed to a tone paired with a foot shock. Their memory for the earlier bad experience is determined based on how much they freeze in response to the "scary" place or sound 24 hr later.
Importantly, the researchers also showed that treatment of animals with a small molecule that increases eIF2a's phosphorylation led to poorer performance on the memory tests.
“These data strengthen the idea that eIF2a phosphorylation is a key, bidirectional point of memory control,?with the ability to turn long-term memory formation on and off, Costa-Mattioli said.
"Taken together, these data strongly support the notion that, under physiological conditions, a decrease in eIF2a phosphorylation constitutes a critical step for the activation of gene expression that leads to the long-term synaptic changes required for memory formation," the researchers concluded. "These findings also raise the interesting possibility that regulators of translation could serve as therapeutic targets for the improvement of memory, for instance in human disorders associated with memory loss."