Scripps Research Institute confirms critical role for microRNAs in development of memory

Finding could implicate a potential drug target for dealing with memory problems in the elderly

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A new study by scientists at the Florida campus of The ScrippsResearch Institute has confirmed a critical role formicroRNAs in the development of memory in the part of the brain calledthe amygdala, which is involved in emotional memory. The new study foundthat a specific microRNA—miR-182—was deeply involved in memoryformation within this brain structure.
"No one had looked at the roleof microRNAs in amygdala memory," said Courtney Miller, a TSRIassistant professor who led the study. "And it looks as though miR-182may be promoting local protein synthesis, helping to support thesynapse-specificity of memories."
In the new study, published in the Journal of Neuroscience, the scientists measured the levels of all known microRNAs following ananimal model of learning. A microarray analysis, which enables rapidgenetic testing on a large scale, showed that more than half of allknown microRNAs are expressed in the amygdala. Seven of those microRNAsincreased and 32 decreased when learning occurred.
The studyfound that, of the microRNAs expressed in the brain, miR-182 had one ofthe lowest levels and these decreased further with learning. Despitethese very low levels, its overexpression prevented the formation ofmemory and led to a decrease in proteins that regulate neuronalplasticity (neurons' ability to adapt) through changes in structure.
Thesefindings suggest that learning-induced suppression of miR-182 is a mainsupporting factor in the formation of long-term memory in the amagdala,as well as an underappreciated mechanism for regulating proteinsynthesis during memory consolidation, Miller said.
Furtheranalysis identified miR-182 as a repressor of proteins that controlactin—a major component of the cytoskeleton, the scaffolding that holdscells together.
"We know that memory formation requires changesin dendritic spines on the neurons through regulation of the actincytoskeleton," Miller said. "When miR-182 is suppressed through learningit halts, at least in part, repression of actin-regulating proteins, sothere's a good chance that miR-182 exerts important control over theactin cytoskeleton."
Miller is now interested in whether or nothigh levels of miR-182 accumulate in the aging brain, something thatwould help to explain a tendency toward memory loss in the elderly. Shealso notes that other research has shown that animal models lackingmiR-182 had no significant physical or cellular abnormalities,suggesting that miR-182 could be a viable target for drug discovery.
The study, "MicroRNA-182 Regulates Amygdala-Dependent Memory Formation," was published in the Jan. 23 issue of The Journal of Neuroscience.
SOURCE: The Scripps Research Institute

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