Discovery of a circuit-specific gene system during sensory plasticity
Groundbreaking approach with local genetic manipulation
Graduate School of Medicine / Faculty of Medicine
The research group of Project Assistant Professor Tadashi Tsubota at the University of Tokyo Graduate School of Medicine has found that the cofilin1 gene, which affects the strength with which neurons bind together, only works in specific neuronal circuits during plastic changes in the rodent cerebral cortex.
"Connectivity" between neurons engaged in various circuits is constantly changing depending on our experience, resulting in plastic changes in cerebral cortical neural connections that are the basis of our learning and memory. Cofilin1 regulates the strength of connections between neurons through physically increasing or decreasing the connection surface between neurons. Although its function has been studied mainly in the hippocampus, its role in the cerebral cortex is still unclear. Specifically, it is essential to identify circuits in which cofilin1 regulates connectivity between neurons.
A region in the cerebral cortex of rats and other rodents represents sensations from the whiskers. Using a rat in which the expression of the cofilin1 gene was suppressed in this region, the researchers artificially blocked sensory stimulus from the whiskers and then induced plastic change in the region. They discovered that cofilin1-mediated morphological changes in neurons was required only for plastic changes that occurred between regions that represent the sensations from individual whiskers.
This new finding will enhance our understanding of cofilin1 function in the cerebral cortex. Furthermore, this research outcome showed an important methodological development; genetic manipulation, which has typically been performed in a wide area of, or throughout, the cerebral cortex, can be restricted to selected neural circuits in the cerebral cortex.
Cofilin1 Controls Transcolumnar Plasticity in Dendritic Spines in Adult Barrel Cortex", PLoS Biology Online Edition: 2015/2/28 (Japan time), doi: 10.1371/journal.pbio.1002070.
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