若手道場

若手道場8

2021/10/1　10:00～11:00　ZOOM 若手道場 WD8-1 ニクジュヨウエキスによる後縦靭帯骨化症モデルマウスの運動機能改善作用 Effects of Cistanche tubulosa extract on motor function in ossification of posterior longitudinal ligament model mice ^○須山真聡, Ximeng Yang, Kaori Nomoto, Chihiro Tohda 富山大学　神経機能学領域 ^○Masato Suyama, Ximeng Yang, Kaori Nomoto, Chihiro Tohda Section of Neuromedical Science, Institute of Natural Medicine, University of Toyama In ossification of posterior longitudinal ligament (OPLL), ectopic ossification of the spinal ligament presses and damages the spinal cord, leading motor dysfunction and pain. Although analgesics are prescribed for complaints of pain, there is no effective medication for recovery of motor function. Our previous study found that Cistanche tubulosa extract improved motor function in chronic phase of spinal cord injury. Expecting therapeutic effect of the extract against OPLL, this study investigated effects of C. tubulosa extract on OPLL model mice. C. tubulosa extract was orally administrated to OPLL model ENPP1^ttw/ttw mice (ttw mice) every day. Motor function was evaluated by Basso mouse scale, Toyama mouse score, Inclined wire mesh climbing test and Narrow bar walking test once every 7 days. Decline of the motor score in Inclined wire mesh climbing test tended to be inhibited by extract treatment. After oral administration of C. tubulosa extract, its major compounds, acteoside and echinacoside, are transferred to at least the cerebral cortex, spinal cord and skeletal muscle. Therefore, we investigated effects of these compounds on neurons and skeletal muscle. Acteoside treatment significantly increased axonal length of cultured cortical neurons. On acteoside-treated cultured myocytes, cultured spinal cord neurons were overlaid. Axonal length of the neurons was significantly increased. This study suggests that after orally administration of C. tubulosa extract, at least acteoside transfers to the central nervous system and skeletal muscle and may enhance axonal growth. Since OPLL patients and ttw mice show axonal damage, we are now evaluating further effects of extract on ttw mice and its acteoside-mediated mechanism.		2021/10/1　10:00～11:00　ZOOM 若手道場 WD8-2 脳梗塞後の自発運動がもたらす脳の組織学的変化 Voluntary exercise induces histological changes in the brain after cerebral ischemia. ^○福本佳永¹, Natsumi Yamaguchi¹, Toshinori Sawano¹, Jin Nakatani¹, Daijiro Yanagisawa², Ikuo Tooyama², Hidekazu Tanaka¹ 1.立命館大学, 2.Molecular Neuroscience Research Center, Shiga University of Medical Science ^○Kae Fukumoto¹, Natsumi Yamaguchi¹, Toshinori Sawano¹, Jin Nakatani¹, Daijiro Yanagisawa², Ikuo Tooyama², Hidekazu Tanaka¹ 1.Department of life science, Ritsumeikan University, 2.Molecular Neuroscience Research Center, Shiga University of Medical Science Previous studies have indicated that exercise promotes functional recovery of C57BL/6middle cerebral artery occlusion (MCAO) mice. However, reliable assessing the effect of exercise after MCAO using C57BL/6 mice is challenging because of the variance of blood vessel running. Currently, to investigate the effects of voluntary running exercise on the brain tissue remodeling, we took advantage of a highly reproducible model of cerebral ischemia using C.B-17/Icr-+/+Jcl mice. Exercise induced functional recovery in grid walking test and wire hang test 14 days after MCAO. There were no significant differences in the infarct size or the number of neurons in the peri-infarct cortex between exercise and non-exercise group, whereas exercise ameliorated MCAO-induced loss of dendritic spine density. Furthermore, the blood vessel area in the peri-infarct cortex was significantly increased by running exercise. Our data suggest the importance of spine density in the functional recovery and supportive effect of the blood vessels on the dendritic spine loss inhibition after cerebral ischemia.

2021/10/1　10:00～11:00　ZOOM 若手道場 WD8-3 デキストラン硫酸ナトリウム誘発性大腸炎が行動開始時の意欲と神経活動に及ぼす影響 Effects of dextran sulfate sodium (DSS)-induced colitis for motivation and neural activity at action initiation ^○河野晏奈¹, Yamaura Katsunori¹, Kenji Tanaka² 1.慶應薬学, 2.Department of Neuropsychiatry, Keio University School of Medicine ^○Anna Kono¹, Yamaura Katsunori¹, Kenji Tanaka² 1.Research Associate Division of Social Pharmacy, Center for Social Pharmacy and Pharmaceutical Care Sciences. Faculty of Pharmacy, Keio University, 2.Department of Neuropsychiatry, Keio University School of Medicine Dorsomedial striatum (DMS) receives inputs from the anterior cingulate cortex (ACC). Although this pathway controls pain in addition to goal-directed behavior, no study has yet tested, at the level of neural activity, whether pain processing modulates motivation for goal-directed behavior. This study addressed this question by recoding population neural activity of DMS dopamine type2 receptor-expressing neurons (D2-MSNs) in mice with visceral pain induced by DSS treatment. To quantify motivation, we used a lever press task where five lever presses were required to attain one reward. Timings of the trial start (TS: levers were presented) were fixed in 30 s after the completion of the preceding trial. For pain induction, the mice were given ad libitum access to DSS-dissolved water for 9 days after the training has finished. We regarded the first lever press latency from TS (LFLP) as an index of motivation; trials with short LFLP were regarded as highly motivated trials and those with long LFLP as unmotivated trials. This enabled us to compare the mice’s motivation before and after the pain induction. Before the pain induction, the averaged Ca2+ levels of DMS D2-MSNs showed zero in z-score around TS and peaked at the first lever press. The trough of the Ca2+ wave was at the reward delivery. After the pain induction, we discovered that unmotivated trials were increased. Although neural activity patterns were similar to pre-pain induction periods, the z-score of compound Ca2+ levels preceding TS tends to be greater than zero in highly motivated trials and smaller than zero in unmotivated trials. Taken together, we propose that the motivation for action initiation is correlated with DMS neural activity and is modulated by pain information signaled via the ACC-DMS pathway.