一般ポスター

一般ポスター情動・行動・生体リズム

7月6日（木）　13:20-14:20　ポスター会場① 1P③-1 シアル酸転移酵素St3gal4欠損マウスにおける不安症―代謝相関 Sialyltransferase St3gal4-deficient mice shows anxiety-metabolism correlation 村田　賢司¹, Siriporn Tangsudjai², 田村　聡哉¹, 藤田　明子¹, 加藤　啓子¹ 1. 京都産業大学大学院　生命科学研究科, 2. Mahidol University,VETERINARY FACULTY Kenji Murata¹, Siriporn Tangsudjai², Toshiya Tamura¹, Akiko Fujita¹, Keiko Kato¹ 1. Division of Life Sciences, Kyoto Sangyo Univ., 2. Mahidol University,VETERINARY FACULTY St3gal4, which synthesizes sugar chains, causes epilepsy, and its deletion is associated with depression and anxiety. The Genome-Wide Association Studies (GWAS) Catalog has shown that single nucleotide polymorphisms in human ST3GAL4 are associated with body size, plasma alkaline phosphatase (ALP) levels, N-glycan protein levels, low-density lipoprotein cholesterol (LDL-C) levels, and serum cholesterol levels. In the present study, we investigated whether St3gal4 exhibits similar metabolic changes to humans and whether these metabolic changes are associated with anxiety-like symptoms: St3gal4-deficient mice, male and female, showed decreased body weight, increased plasma ALP levels and decreased tryptophan and total cholesterol levels, which included human ST3GAL4-related metabolites that the GWAS catalog shows. In addition, female mice also showed reduced levels of very-low-density lipoprotein cholesterol VLDL-C, suggesting that ST3GAL4 is involved in similar metabolic systems between humans and mice. St3gal4-deficient mice showed a correlation between plasma ALP and the tone fear levels in the fear conditioning test and a marked decrease of ALP activity in the thalamus. It suggests that the St3gal4-ALP axis is involved in the coexistence of emotional behavior and metabolism in the central and peripheral systems.		7月6日（木）　13:20-14:20　ポスター会場① 1P③-2 mCherry標識シアル酸転移酵素St3gal4が関わる可塑的変化の3次元脳観察 3D brain imaging of plastic changes related to St3gal4 in mCherry-labeled neurons 森井　渉羽¹, 上村　碧¹, 田村　聡哉¹, Siriporn Tangsudjai^1,2, 藤田　明子¹, 伊川　正人³, 野中　茂紀⁴, 加藤　啓子¹ 1. 京都産業大学大学院　生命科学研究科（生命科学部）, 2. Mahidol University VETERINARY FACULTY, 3. 大阪大学　微生物病研究所, 4. 基礎生物学研究所　生命創成探究センター　時空間制御研究室 Ayuha Morii¹, Aoi Uemura¹, Toshiya Tamura¹, Siriporn Tangsudjai^1,2, Akiko Fujita¹, Masahito Ikawa³, Shigenori Nonaka⁴, Keiko Kato¹ 1. Division of Life Sciences, Kyoto Sangyo Univ., 2. Mahidol University VETERINARY FACULTY, 3. RIMD, Osaka Univ., 4. Laboratory for Spatiotemporal Regulations, ExCLEES, NIBB A sialyltransferase, St3gal4, is a causative gene in amygdala-kindling mice, a temporal lobe epilepsy model. In the present study, we aim to study how sialic acid modifications by St3gal4 in the thalamus modulate plastic changes in neural circuits, which leads to epilepsy or depression and anxiety. To visualize the plastic changes that occur when neurons expressing St3gal4 exhibit epileptic seizures and anxiety, we established St3gal4^mCherry (St3gal4^+/- expressing mCherry) knock-in mice, in which the targeting vector consists of a mCherry cassette followed by a CRISPER/Cas system inserted in frame into Exon 3. Kindling stimuli into the basolateral amygdala induced epileptic seizures in St3gal4^mCherry/+ knock-in (KI) mice (St3gal4-KIWT) but not in St3gal4^mCherry/- KI mice (St3gal4-KIKO). Next, the whole-brain 3D images were collected by light-sheet microscopy. The regions that mCherry-positive neurons and the projections distributed were almost the same in both mice, regardless of the expression of St3gal4. In both cases, mCherry was observed in neurons on the cerebellar-thalamic circuit and the thalamocortical transmission pathway via Papez's route. To understand the nature of mCherry-labeled neurons and the neurons at the projection site, we are currently observing their associations with neurons, including inhibitory neuronal markers and dopamine- and serotonin receptors.

7月6日（木）　13:20-14:20　ポスター会場① 1P③-3 Exploration of physiological functions of the septin cytoskeleton in thecerebellum 後藤　直樹, 鳥居　紗帆, 西川　将司, 木下　専名古屋大学　理学研究科　理学専攻　生命理学領域 Naoki Goto, Masashi Nishikawa, Masashi Nishikawa, Makoto Kinoshita Dept. of Science, Nagoya University Septins (SEPT1-14), a family of polymerizing GTPases, are implicated in diverse cellular processes as a component of the membrane skeleton, cytoskeletal network beneath the plasma membrane (Kinoshita et al., J Comp Neurol 2000). In the cerebellar cortex, septin hetero-oligomers abound in the membrane skeleton of Purkinje cell (PC) dendrites and Bergmann glial (BG) processes. The glial subset interacts with two glia selective proteins, CDC42EP4 (a CDC42 effector) and GLAST/EAAT1 (a glutamate transporter), in the perisynaptic lamellar processes of BG. Although Cdc42ep4-KO mice manifest motor coordination/learning defects due to insufficiency of GLAST-mediated glutamate clearance (Ageta-Ishihara et al., Nat Commun 2015), lack of direct evidence on the loss-of-function phenotypes of septins limits our understanding of their molecular functions in the cerebellar neurons and glia. To address this, we attempt cell-selective knockout of one of the core subunits by using floxed mouse lines, and neuron/glia-selective expression of Cre recombinase via in utero electroporation and pre/postnatal transduction of adeno-associated viral vectors, followed by physiological, histological, and biochemical analyses. We expect the time/cost-efficient approach to reveal loss-of-function phenotypes of septins and related proteins in the cerebellum and other brain regions.		7月6日（木）　13:20-14:20　ポスター会場① 1P③-4 セロトニンによる自発行動制御 Serotonergic regulation of locomotor activity 畦地　裕統, 高橋　晋同志社大学脳科学研究科認知行動神経機構部門 Hirotsugu Azechi, Susumu Takahashi Laboratory of Cognitive and Behavioral Neuroscience, Graduate School of Brain Science, Doshisha University Serotonin is thought to regulate various behaviors and mental functions, but its mechanisms remain unclear. The Fawn-hooded (FH) rat substrain FH/HamSlc exhibits behavioral hyperactivity and reduced serotonin in the prefrontal cortex and hippocampus. Therefore, focusing on the relationship between serotonin and locomotor activity, we investigated whether pharmacological manipulation of serotonin levels alters locomotor activity in FH/HamSlc. The experiment was conducted using a within-subject design with six FH/HamSlc. 5-hydroxytryptophan (5-HTP), an immediate serotonin precursor, or 4-chloro-DL-phenylalanine methyl ester hydrochloride (pCPA), an inhibitor of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, were administered followed by an open field test 1 hour later. The results showed that 5-HTP, which induces serotonin synthesis, suppressed locomotor activity, and pCPA, which induces serotonin depletion, also suppressed locomotor activity. This suppression of locomotor activity by pCPA was not rescued by 5-HTP. These results suggest that the serotonergic system influences locomotor activity, but its effects do not depend on serotonin levels. Based on these results, we are further analyzing the regulatory mechanisms of the serotonergic system on locomotor activity using pharmacology, optogenetics, and in vivo electrophysiology.

7月6日（木）　13:20-14:20　ポスター会場① 1P③-5 思春期社会隔離マウスの社会性と内側眼窩前頭葉-扁桃体シナプス異常に対する再社会化飼育の改善効果の臨界期 Critical period for effects of resocialization on social isolation-induced social and the OFC-amygdala synaptic deficits 國石　洋^1,2, 山田　光彦², 松崎　秀夫¹ 1. 福井大学　子どものこころ　脳機能発達, 2. 国立精神・神経医療研究センター　精神保健研究所　精神薬理研究部 Hiroshi Kuniishi^1,2, Mitsuhiko Yamada², Hideo Mastuzaki¹ 1. Div. of Development of Mental Functions, Research Center for Child Mental Development, Univ. of Fukui, Fukui, Japan Japan., 2. Dept.of Neuropsychopharmacol., National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan. Early social experiences impact on development of social function, and early-life social isolation (SI) induces social deficit in animals and human. Especially, in rodents, early-adolescence is critical period that SI induces social deficit, but not late-adolescence or later. Besides, it has been reported that late-adolescent resocialization (RS, housing with group-reared mice) rescues SI-induced social deficit. However, critical period for effects of RS remains less understood. In this study, to explore the critical period for RS, we examined effects of adolescent or adult RS on SI-induced social deficit. First, we isolated mice during early-adolescence (3-5 weeks of age) and examined the effect of late-adolescent RS (6-9 weeks of age). As previous reports, late-adolescent RS rescued SI-induced social deficit. Then, we isolated mice during adolescence (3-8 weeks of age) and examined the effect of adult RS (9-12 weeks of age). Contrary to late-adolescent RS, adult RS did not rescue SI-induced social deficit. In addition, these behavioral changes were associated with functional change in the medial orbitofrontal-basolateral amygdala (mOFC-BLA) synaptic function which is involved in modulation of social behavior. These results suggested that the critical period for restorative effect of RS on SI-induced social and the mOFC-BLA synaptic deficits is limited until late-adolescence.		7月6日（木）　13:20-14:20　ポスター会場① 1P③-6 時計遺伝子による一次繊毛形態制御機構の解析 Clock genes regulate morphology of primary cilia 中里　亮太, 松田　悠生, 木曽　遼太郎, 池上　浩司広島大学　医系科学研究科　解剖学及び発生生物学研究室 Ryota Nakazato, Yuki Matsuda, Ryotarou Kiso, Koji Ikegami Dept. Anatomy and Developmental Biology, Univ. of Hiroshima, Hiroshima, Japan Various biological phenomena, including the sleep/wake cycle, exhibit circadian rhythms. This system is generated by the oscillating expression of clock genes in approximately 24-hour cycle. Primary cilia, a small organelle protruding from the cell surface, functions as a sensory antenna for cells to detect extracellular signals. In this study, we attempted to evaluate the relationship between circadian rhythms and primary cilia. NIH/3T3 mouse embryonic fibroblasts were treated with 100 nM dexamethasone (DEX) for synchronize the expression rhythm of clock genes, and then cells were fixed with 4% paraformaldehyde (PFA) every 6 hours. Visualization of primary cilia by immunostaining revealed that the length of primary cilia in NIH/3T3 cells exposed to DEX exhibited oscillations with a 24-hour cycle, which were suppressed by SR9011, an agonist of the clock gene repressor REV-ERB. In C57BL/6 mice, brains were also collected after intracardial perfusion with 4% PFA every 6 hours. Visualization of primary cilia in the brain by immunostaining revealed a circadian rhythms in the length of primary cilia similar to that observed in cultured cells. These results suggest that the length of primary cilia is regulated by clock genes and exhibits circadian rhythms.