Hideo Mukai

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.

TL;DR: Two types of independent synaptic plasticity, long‐term depression and spinogenesis, were investigated, in response to 17β‐estradiol and agonists of estrogen receptors using hippocampal slices from adult male rats, and it was demonstrated that estradiol rapidly enhanced LTD not only in CA1 but also in CA3 and dentate gyrus.

TL;DR: Estrogen modulates memory-related synaptic plasticity not only slowly but also rapidly in the hippocampus, and ERalpha, but not ERbeta, induces the same enhancement/suppression effects on both spinogenesis and LTD.

TL;DR: It is suggested that male hippocampal E2 synthesis pathway may be androstenedione --> T --> E2 or dehydroepiandrosterone --> and Frostenediol --> T ― E2 but not androstensione --> E1 --> E 2.

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.