Search

Your search keyword '"Mizuta K"' showing total 1,136 results
Start Over Author "Mizuta K"
1,136 results on '"Mizuta K"'

21. Distinct Mechanisms of Over-Representation of Landmarks and Rewards in the Hippocampus

Author

Japan Science and Technology Agency, Ministry of Education, Culture, Sports, Science and Technology (Japan), Senshin Medical Research Foundation, Human Frontier Science Program, Fujitsu, Japan Agency for Medical Research and Development, Volkswagen Foundation, Ministry for Science and Culture of Lower Saxony, Sato, M., Mizuta, K., Islam, T., Kawano, M., Sekine, Y., Takekawa, T., Gómez-Domínguez, Daniel, Schmidt, A., Wolf, F., Kim, K., Yamakawa, H., Ohkura, M., Lee, M.G., Fukai, T., Nakai, J., Hayashi, Yasunori, Japan Science and Technology Agency, Ministry of Education, Culture, Sports, Science and Technology (Japan), Senshin Medical Research Foundation, Human Frontier Science Program, Fujitsu, Japan Agency for Medical Research and Development, Volkswagen Foundation, Ministry for Science and Culture of Lower Saxony, Sato, M., Mizuta, K., Islam, T., Kawano, M., Sekine, Y., Takekawa, T., Gómez-Domínguez, Daniel, Schmidt, A., Wolf, F., Kim, K., Yamakawa, H., Ohkura, M., Lee, M.G., Fukai, T., Nakai, J., and Hayashi, Yasunori

Abstract

In the hippocampus, locations associated with salient features are represented by a disproportionately large number of neurons, but the cellular and molecular mechanisms underlying this over-representation remain elusive. Using longitudinal calcium imaging in mice learning to navigate in virtual reality, we find that the over-representation of reward and landmark locations are mediated by persistent and separable subsets of neurons, with distinct time courses of emergence and differing underlying molecular mechanisms. Strikingly, we find that in mice lacking Shank2, an autism spectrum disorder (ASD)-linked gene encoding an excitatory postsynaptic scaffold protein, the learning-induced over-representation of landmarks was absent whereas the over-representation of rewards was substantially increased, as was goal-directed behavior. These findings demonstrate that multiple hippocampal coding processes for unique types of salient features are distinguished by a Shank2-dependent mechanism and suggest that abnormally distorted hippocampal salience mapping may underlie cognitive and behavioral abnormalities in a subset of ASDs.Using longitudinal two-photon calcium imaging in mice during virtual navigation, Sato et al. demonstrate that persistent and separable neuronal subsets mediate the hippocampal over-representation of reward and landmark locations. Learning-induced over-representation of landmarks is absent while rapid over-representation of rewards is enhanced, in a mouse model of autism lacking Shank2.

Published
2020

Catalog

Books, media, physical & digital resources
See catalog results