T
Taka-aki Hattori
Researcher at University of Tokyo
Publications - 3
Citations - 974
Taka-aki Hattori is an academic researcher from University of Tokyo. The author has contributed to research in topics: Hippocampal formation & Pregnenolone. The author has an hindex of 3, co-authored 3 publications receiving 934 citations.
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Journal ArticleDOI
Adult male rat hippocampus synthesizes estradiol from pregnenolone by cytochromes P45017α and P450 aromatase localized in neurons
Yasushi Hojo,Taka-aki Hattori,Taihei Enami,A. Furukawa,Kumiko Suzuki,Hirotaka Ishii,Hideo Mukai,John H. Morrison,William G.M. Janssen,Shiro Kominami,Nobuhiro Harada,Tetsuya Kimoto,Suguru Kawato +12 more
TL;DR: Results imply that 17beta-estradiol is synthesized by P45017alpha and P450 aromatase localized in hippocampal neurons from endogenous cholesterol, and may be regulated by a glutamate-mediated synaptic communication that evokes Ca(2+) signals.
Journal ArticleDOI
Corticosterone acutely prolonged N-methyl-d-aspartate receptor-mediated Ca2+ elevation in cultured rat hippocampal neurons.
Taiki Takahashi,Tetsuya Kimoto,Nobuaki Tanabe,Taka-aki Hattori,Nobuaki Yasumatsu,Suguru Kawato +5 more
TL;DR: The results imply that high levels of CORT induce a rapid and non‐genomic prolongation of NMDA receptor‐mediated Ca2+ elevation, probably via putative membrane surface receptors for CORT in the hippocampal neurons.
Journal ArticleDOI
Hippocampal cytochrome P450s synthesize brain neurosteroids which are paracrine neuromodulators of synaptic signal transduction.
Keisuke Shibuya,Norio Takata,Yasushi Hojo,A. Furukawa,Nobuaki Yasumatsu,Tetsuya Kimoto,Taihei Enami,Kumiko Suzuki,Nobuaki Tanabe,Hirotaka Ishii,Hideo Mukai,Taiki Takahashi,Taka-aki Hattori,Suguru Kawato +13 more
TL;DR: Hippocampal pyramidal neurons and granule neurons of adult male rats are equipped with a complete machinery for the synthesis of pregnenolone, dehydroepiandrosterone, 17beta-estradiol and testosterone as well as their sulfate esters, promising neuromodulators that may either activate or inactivate neuron-neuron communication, thereby mediating learning and memory in the hippocampus.