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Muneki Ikeda Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Yasushi Hojo Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Yoshimasa Komatsuzaki Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Masahiro Okamoto Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Asami Kato Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Taishi Takeda Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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Suguru Kawato Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan

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The corticosterone (CORT) level changes along the circadian rhythm. Hippocampus is sensitive to CORT, since glucocorticoid receptors are highly expressed. In rat hippocampus fixed in a living state every 3 h, we found that the dendritic spine density of CA1 pyramidal neurons increased upon waking (within 3 h), as compared with the spine density in the sleep state. Particularly, the large-head spines increased. The observed change in the spine density may be due to the change in the hippocampal CORT level, since the CORT level at awake state (∼30 nM) in cerebrospinal fluid was higher than that at sleep state (∼3 nM), as observed from our earlier study. In adrenalectomized (ADX) rats, such a wake-induced increase of the spine density disappeared. S.c. administration of CORT into ADX rats rescued the decreased spine density. By using isolated hippocampal slices, we found that the application of 30 nM CORT increased the spine density within 1 h and that the spine increase was mediated via PKA, PKC, ERK MAPK, and LIMK signaling pathways. These findings suggest that the moderately rapid increase of the spine density on waking might mainly be caused by the CORT-driven kinase networks.

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