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嶋田 逸誠シマダ イッセイ

所属部署医学研究科細胞生化学分野
職名講師
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Last Updated :2020/06/02

研究者基本情報

学歴

  • 2005年08月 - 2010年05月, バーモント大学大学院, 医学部
  • 2002年04月 - 2004年03月, 兵庫県立大学大学院, 理学部
  • 1998年04月 - 2002年03月, 兵庫県立大学, 理学部

学位

  • PhD, University of Vermont

所属学協会

  • 日本分子生物学会

経歴

  •   2018年08月 - 現在, 名古屋市立大学, 医学研究科細胞生化学分野, 講師
  •   2015年01月 - 2018年07月, テキサス大学サウスウエスタン校 メディカルセンター, 細胞生物学部, アシスタントインストラクター
  •   2011年08月 - 2014年12月, テキサス大学サウスウエスタン校 メディカルセンター, ポスドク
  •   2010年04月 - 2011年07月, バーモント大学大学院, 医学部, ポスドク

研究活動情報

研究分野

  • ライフサイエンス, 細胞生物学
  • ライフサイエンス, 発生生物学
  • ライフサイエンス, 神経形態学
  • ライフサイエンス, 解剖学

研究キーワード

    神経発生, 転写因子, 神経前駆細胞, 上衣細胞, 水頭症, 神経産生, アストロサイト, 自己複製能, 分化, 髄芽腫, 神経幹細胞, 繊毛, 神経科学

論文

  • Derepression of sonic hedgehog signaling upon Gpr161 deletion unravels forebrain and ventricular abnormalities., Developmental Biology, 450, (1) 47 - 62,   2019年06月, 査読有り
  • Basal Suppression of the Sonic Hedgehog Pathway by the G-Protein-Coupled Receptor Gpr161 Restricts Medulloblastoma Pathogenesis., Shimada IS, Hwang SH, Somatilaka BN, Wang X, Skowron P, Kim J, Kim M, Shelton JM, Rajaram V, Xuan Z, Taylor MD, Mukhopadhyay S, Cell reports, 22, (5) 1169 - 1184,   2018年01月, 査読有り
  • Prdm16 is required for the maintenance of neural stem cells in the postnatal forebrain and their differentiation into ependymal cells, Issei S. Shimada, Melih Acar, Rebecca J. Burgess, Zhiyu Zhao, Sean J. Morrison, GENES & DEVELOPMENT, 31, (11) 1134 - 1146,   2017年06月, 査読有り, We and others showed previously that PR domain-containing 16 (Prdm16) is a transcriptional regulator required for stemcell function in multiple fetal and neonatal tissues, including the nervous system. However, Prdm16 germline knockout mice died neonatally, preventing us from testing whether Prdm16 is also required for adult stem cell function. Here we demonstrate that Prdm16 is required for neural stem cell maintenance and neurogenesis in the adult lateral ventricle subventricular zone and dentate gyrus. We also discovered that Prdm16 is required for the formation of ciliated ependymal cells in the lateral ventricle. Conditional Prdm16 deletion during fetal development using Nestin-Cre prevented the formation of ependymal cells, disrupting cerebrospinal fluid flow and causing hydrocephalus. Postnatal Prdm16 deletion using Nestin-CreERT2 did not cause hydrocephalus or prevent the formation of ciliated ependymal cells but caused defects in their differentiation. Prdm16 was required in neural stem/progenitor cells for the expression of Foxj1, a transcription factor that promotes ependymal cell differentiation. These studies show that Prdm16 is required for adult neural stem cell maintenance and neurogenesis as well as the formation of ependymal cells.
  • Using Primary Neurosphere Cultures to Study Primary Cilia, Issei S. Shimada, Hemant Badgandi, Bandarigoda N. Somatilaka, Saikat Mukhopadhyay, JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, (122) ,   2017年04月, 査読有り, The primary cilium is fundamentally important for the proliferation of neural stem/progenitor cells and for neuronal differentiation during embryonic, postnatal, and adult life. In addition, most differentiated neurons possess primary cilia that house signaling receptors, such as G-protein-coupled receptors, and signaling molecules, such as adenylyl cyclases. The primary cilium determines the activity of multiple developmental pathways, including the sonic hedgehog pathway during embryonic neuronal development, and also functions in promoting compartmentalized subcellular signaling during adult neuronal function. Unsurprisingly, defects in primary cilium biogenesis and function have been linked to developmental anomalies of the brain, central obesity, and learning and memory deficits. Thus, it is imperative to study primary cilium biogenesis and ciliary trafficking in the context of neural stem/progenitor cells and differentiated neurons. However, culturing methods for primary neurons require considerable expertise and are not amenable to freeze-thaw cycles. In this protocol, we discuss culturing methods for mixed populations of neural stem/progenitor cells using primary neurospheres. The neurosphere-based culturing methods provide the combined benefits of studying primary neural stem/progenitor cells: amenability to multiple passages and freeze-thaw cycles, differentiation potential into neurons/glia, and transfectability. Importantly, we determined that neurosphere-derived neural stem/progenitor cells and differentiated neurons are ciliated in culture and localize signaling molecules relevant to ciliary function in these compartments. Utilizing these cultures, we further describe methods to study ciliogenesis and ciliary trafficking in neural stem/progenitor cells and differentiated neurons. These neurosphere-based methods allow us to study cilia-regulated cellular pathways, including G-protein-coupled receptor and sonic hedgehog signaling, in the context of neural stem/progenitor cells and differentiated neurons.
  • Tubby family proteins are adapters for ciliary trafficking of integral membrane proteins, Hemant B. Badgandi, Sun-hee Hwang, Issei S. Shimada, Evan Loriot, Saikat Mukhopadhyay, JOURNAL OF CELL BIOLOGY, 216, (3) 743 - 760,   2017年03月, 査読有り, The primary cilium is a paradigmatic organelle for studying compartmentalized signaling; however, unlike soluble protein trafficking, processes targeting integral membrane proteins to cilia are poorly understood. In this study, we determine that the tubby family protein TULP3 functions as a general adapter for ciliary trafficking of structurally diverse integral membrane cargo, including multiple reported and novel rhodopsin family G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex. The founding tubby family member TUB also localizes to cilia similar to TULP3 and determines trafficking of a subset of these GPCRs to neuronal cilia. Using minimal ciliary localization sequences from GPCRs and fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs to be sufficient and TULP3 dependent for ciliary trafficking. We propose a three-step model for TULP3/TUB-mediated ciliary trafficking, including the capture of diverse membrane cargo by the tubby domain in a phosphoinositide 4,5-bisphosphate (PI(4,5) P-2)-dependent manner, ciliary delivery by intraflagellar transport complex A binding to the TULP3/TUB N terminus, and subsequent release into PI(4,5) P-2-deficient ciliary membrane.
  • G-Protein-Coupled Receptor Signaling and Neural Tube Closure Defects, Issei S. Shimada, Saikat Mukhopadhyay, BIRTH DEFECTS RESEARCH, 109, (2) 129 - 139,   2017年01月, 査読有り, Disruption of the normal mechanisms that mediate neural tube closure can result in neural tube defects (NTDs) with devastating consequences in affected patients. With the advent of next-generation sequencing, we are increasingly detecting mutations in multiple genes in NTD cases. However, our ability to determine which of these genes contribute to the malformation is limited by our understanding of the pathways controlling neural tube closure. G-protein-coupled receptors (GPCRs) comprise the largest family of transmembrane receptors in humans and have been historically favored as drug targets. Recent studies implicate several GPCRs and downstream signaling pathways in neural tube development and closure. In this review, we will discuss our current understanding of GPCR signaling pathways in pathogenesis of NTDs. Notable examples include the orphan primary cilialocalized GPCR, Gpr161 that regulates the basal suppression machinery of sonic hedgehog pathway by means of activation of cAMP-protein kinase A signaling in the neural tube, and protease-activated receptors that are activated by a local network of membrane-tethered proteases during neural tube closure involving the surface ectoderm. Understanding the role of these GPCR-regulated pathways in neural tube development and closure is essential toward identification of underlying genetic causes to prevent NTDs. (C) 2016 Wiley Periodicals, Inc.
  • Trafficking to the primary cilium membrane, Saikat Mukhopadhyay, Hemant B. Badgandi, Sun-hee Hwang, Bandarigoda Somatilaka, Issei S. Shimada, Kasturi Pal, MOLECULAR BIOLOGY OF THE CELL, 28, (2) 233 - 239,   2017年01月, 査読有り, The primary cilium has been found to be associated with a number of cellular signaling pathways, such as vertebrate hedgehog signaling, and implicated in the pathogenesis of diseases affecting multiple organs, including the neural tube, kidney, and brain. The primary cilium is the site where a subset of the cell's membrane proteins is enriched. However, pathways that target and concentrate membrane proteins in cilia are not well understood. Processes determining the level of proteins in the ciliary membrane include entry into the compartment, removal, and retention by diffusion barriers such as the transition zone. Proteins that are concentrated in the ciliary membrane are also localized to other cellular sites. Thus it is critical to determine the particular role for ciliary compartmentalization in sensory reception and signaling pathways. Here we provide a brief overview of our current understanding of compartmentalization of proteins in the ciliary membrane and the dynamics of trafficking into and out of the cilium. We also discuss major unanswered questions regarding the role that defects in ciliary compartmentalization might play in disease pathogenesis. Understanding the trafficking mechanisms that underlie the role of ciliary compartmentalization in signaling might provide unique approaches for intervention in progressive ciliopathies.
  • Leptin Receptor Promotes Adipogenesis and Reduces Osteogenesis by Regulating Mesenchymal Stromal Cells in Adult Bone Marrow, Rui Yue, Bo O. Zhou, Issei S. Shimada, Zhiyu Zhao, Sean J. Morrison, CELL STEM CELL, 18, (6) 782 - 796,   2016年06月, 査読有り, Skeletal stem cells (SSCs) that are the major source of osteoblasts and adipocytes in adult bone marrow express leptin receptor (LepR). To test whether LepR regulates SSC function, we conditionally deleted Lepr from limb bone marrow stromal cells, but not from the axial skeleton or hypothalamic neurons, using Prx1-Cre. Prx1-Cre;Lepr(fl/fl) mice exhibited normal body mass and normal hematopoiesis. However, limb bones from Prx1-Cre;Lepr(fl/fl) mice exhibited increased osteogenesis, decreased adipogenesis, and accelerated fracture healing. Leptin increased adipogenesis and reduced osteogenesis by activating Jak2/Stat3 signaling in bone marrow stromal cells. A high-fat diet increased adipogenesis and reduced osteogenesis in limb bones from wild-type mice, but not from Prx1-Cre;Lepr(fl/fl) mice. This reflected local effects of LepR on osteogenesis and adipogenesis by bone marrow stromal cells and systemic effects on bone resorption. Leptin/LepR signaling regulates adipogenesis and osteogenesis by mesenchymal stromal cells in the bone marrow in response to diet and adiposity.
  • Notch1-STAT3-ETBR signaling axis controls reactive astrocyte proliferation after brain injury., LeComte MD, Shimada IS, Sherwin C, Spees JL, Proceedings of the National Academy of Sciences of the United States of America, 112, (28) 8726 - 8731,   2015年07月, 査読有り
  • Self-Renewal and Differentiation of Reactive Astrocyte-Derived Neural Stem/Progenitor Cells Isolated from the Cortical Peri-Infarct Area after Stroke, Issei S. Shimada, Matthew D. LeComte, Jerrica C. Granger, Noah J. Quinlan, Jeffrey L. Spees, JOURNAL OF NEUROSCIENCE, 32, (23) 7926 - 7940,   2012年06月, 査読有り, In response to stroke, subpopulations of cortical reactive astrocytes proliferate and express proteins commonly associated with neural stem/progenitor cells such as glial fibrillary acidic protein (GFAP) and Nestin. To examine the stem cell-related properties of cortical reactive astrocytes after injury, we generated GFAP-CreER (TM);tdRFP mice to permanently label reactive astrocytes. We isolated cells from the cortical peri-infarct area 3 d after stroke, and cultured them in neural stem cell medium containing epidermal growth factor and basic fibroblast growth factor. We observed tdRFP-positive neural spheres in culture, suggestive of tdRFP-positive reactive astrocyte-derived neural stem/progenitor cells (Rad-NSCs). Cultured Rad-NSCs self-renewed and differentiated into neurons, astrocytes, and oligodendrocytes. Pharmacological inhibition and conditional knock-out mouse studies showed that Presenilin 1 and Notch 1 controlled neural sphere formation by Rad-NSCs after stroke. To examine the self-renewal and differentiation potential of Rad-NSCs in vivo, Rad-NSCs were transplanted into embryonic, neonatal, and adult mouse brains. Transplanted Rad-NSCs were observed to persist in the subventricular zone and secondary Rad-NSCs were isolated from the host brain 28 d after transplantation. In contrast with neurogenic postnatal day 4 NSCs and adult NSCs from the subventricular zone, transplanted Rad-NSCs differentiated into astrocytes and oligodendrocytes, but not neurons, demonstrating that Rad-NSCs had restricted differentiation in vivo. Our results indicate that Rad-NSCs are unlikely to be suitable for neuronal replacement in the absence of genetic or epigenetic modification.
  • Proliferating Reactive Astrocytes Are Regulated by Notch-1 in the Peri-Infarct Area After Stroke, Issei S. Shimada, Alyssa Borders, Alexander Aronshtam, Jeffrey L. Spees, STROKE, 42, (11) 3231 - U490,   2011年11月, 査読有り, Background and Purpose-The formation of reactive astrocytes is common after central nervous system injuries such as stroke. However, the signaling pathway(s) that control astrocyte formation and functions are poorly defined. We assess the effects of Notch 1 signaling in peri-infarct-reactive astrocytes after stroke. Methods-We examined reactive astrocyte formation in the peri-infarct area 3 days after distal middle cerebral artery occlusion with or without gamma-secretase inhibitor treatment. To directly study the effects of inhibiting a gamma-secretase cleavage target in reactive astrocytes, we generated glial fibrillary acidic protein-CreER (TM): Notch 1 conditional knockout mice. Results-Gamma-secretase inhibitor treatment after stroke decreased the number of proliferative glial fibrillary acidic protein-positive reactive astrocytes and RC2-positive reactive astrocytes directly adjacent to the infarct core. The decrease in reactive astrocytes correlated with an increased number of CD45-positive cells that invaded into the peri-infarct area. To study the influence of reactive astrocytes on immune cell invasion, ex vivo immune cell invasion assays were performed. We found that a gamma-secretase-mediated pathway in astrocytes affected Jurkat cell invasion. After tamoxifen treatment, glial fibrillary acidic protein-CreER (TM): Notch 1 conditional knockout mice had a significantly decreased number of proliferating reactive astrocytes and RC2-positive reactive astrocytes. Tamoxifen treatment also led to an increased number of CD45-positive cells that invaded the peri-infarct area. Conclusions-Our results demonstrate that proliferating and RC2-positive reactive astrocytes are regulated by Notch 1 signal transduction and control immune cell invasion after stroke. (Stroke. 2011; 42:3231-3237.)
  • SDF-1α secreted by human CD133-derived multipotent stromal cells promotes neural progenitor cell survival through CXCR7., Bakondi B, Shimada IS, Peterson BM, Spees JL, Stem cells and development, 20, (6) 1021 - 1029,   2011年06月, 査読有り
  • Stem and Progenitor Cells for Neurological Repair: Minor Issues, Major Hurdles, and Exciting Opportunities for Paracrine-Based Therapeutics, Issei S. Shimada, Jeffrey L. Spees, JOURNAL OF CELLULAR BIOCHEMISTRY, 112, (2) 374 - 380,   2011年02月, 査読有り, The transplantation of cultured stem and progenitor cells is a key element in the rapidly growing field of regenerative medicine. Based on their ability to rescue and/or repair injured tissue and partially restore organ function, multiple types of stem/progenitor cells have already entered into clinical trials. However, despite several decades of intense research, the goal to apply culture-expanded stem/progenitor cells in a manner that can effectively replace cells after injury has yet to be realized. Many sources of potentially useful cells are available, but something is clearly missing. In addition, recent studies suggest that paracrine effects of secreted or released factors are responsible for most of the benefits observed after cell transplantation, rather than direct cell replacement. These data call into question the need for cell transplantation for many types of therapy, in particular for acute injuries such as myocardial infarction and stroke. In this review, we examine current progress in the area of cell transplantation and minor issues and major hurdles regarding the clinical application of different cell types. We discuss the "paracrine hypothesis" for the action of transplanted stem/progenitor cells as an opportunity to identify defined combinations of biomolecules to rescue and/or repair tissues after injury. Although many of the concepts in this review will apply to multiple injury/repair systems, we will focus primarily on stem/progenitor cell-based treatments for neurological disorders and stroke. J. Cell. Biochem. 112: 374-380, 2011. (C) 2010 Wiley-Liss. Inc.
  • Isolation of Locally Derived Stem/Progenitor Cells From the Peri-Infarct Area That Do Not Migrate From the Lateral Ventricle After Cortical Stroke, Issei S. Shimada, Brittni M. Peterson, Jeffrey L. Spees, STROKE, 41, (9) E552 - E560,   2010年09月, 査読有り, Background and Purpose-Neurogenesis can arise from neural stem/progenitor cells of the subventricular zone after strokes involving both the cortex and striatum. However, it is controversial whether all types of stroke and strokes of different sizes activate neurogenesis from the subventricular zone niche. In contrast with cortical/striatal strokes, repair and remodeling after mild cortical strokes may involve to a greater extent local cortical stem/progenitor cells and cells from nonneurogenic niches. Methods-We compared stem/progenitor cell responses after focal cortical strokes produced by distal middle cerebral artery occlusion and cortical/striatal strokes produced by the intraluminal suture model. To label migrating neuroblasts from the subventricular zone, we injected DiI to the lateral ventricle after distal middle cerebral artery occlusion. By immunohistochemistry, we characterized cells expressing stem/progenitor cell markers in the peri-infarct area. We isolated cortical stem/progenitor cells from the peri-infarct area after distal middle cerebral artery occlusion and assayed their self-renewal and differentiation capacity. Results-In contrast with cortical/striatal strokes, focal cortical strokes did not induce neuroblast migration from the subventricular zone to the infarct zone after distal middle cerebral artery occlusion. By immunohistochemistry, we observed subpopulations of reactive astrocytes in the peri-infarct area that coexpressed radial glial cell markers such as Sox2, Nestin, and RC2. Clonal neural spheres isolated from the peri-infarct area after distal middle cerebral artery occlusion differentiated into neurons, astrocytes, oligodendrocytes, and smooth muscle cells. Notably, neural spheres isolated from the peri-infarct area also expressed RC2 before differentiation. Conclusions-Mild cortical strokes that do not penetrate the striatum activate local cortical stem/progenitor cells but do not induce neuroblast migration from the subventricular zone niche. (Stroke. 2010;41:e552-e560.)
  • CD133 Identifies a Human Bone Marrow Stem/Progenitor Cell Sub-population With a Repertoire of Secreted Factors That Protect Against Stroke, Benjamin Bakondi, Issei S. Shimada, Anthony Perry, James R. Munoz, Joni Ylostalo, Alan B. Howard, Carl A. Gregory, Jeffrey L. Spees, MOLECULAR THERAPY, 17, (11) 1938 - 1947,   2009年11月, 査読有り, The reparative properties of bone marrow stromal cells (BMSCs) have been attributed in part to the paracrine action of secreted factors. We isolated typical human BMSCs by plastic adherence and compared them with BMSC sub-populations isolated by magnetic-activated cell sorting against CD133 (CD133-derived BMSCs, CD133BMSCs) or CD271 [p75 low-affinity nerve growth factor receptor (p75LNGFR), p75BMSCs]. Microarray assays of expressed genes, and enzyme-linked immunosorbent assays (ELISAs) of selected growth factors and cytokines secreted under normoxic and hypoxic conditions demonstrated that the three transit-amplifying progenitor cell populations were distinct from one another. CD133BMSC-conditioned medium (CdM) was superior to p75BMSC CdM in protecting neural progenitor cells against cell death during growth factor/nutrient withdrawal. Intracardiac (arterial) administration of concentrated CD133BMSC CdM provided neuroprotection and significantly reduced cortical infarct volumes in mice following cerebral ischemia. In support of the paracrine hypothesis for BMSC action, intra-arterial infusion of CD133BMSC CdM provided significantly greater protection against stroke compared with the effects of CD133BMSC (cell) administration. CdM from CD133BMSCs also provided superior protection against stroke compared with that conferred by CdM from p75BMSCs or typically isolated BMSCs. CD133 identifies a sub- population of nonhematopoietic stem/progenitor cells from adult human bone marrow, and CD133BMSC CdM may provide neuroprotection for patients with stroke.
  • Effects of diabetes and insulin on the expression of galanin-like peptide in the hypothalamus of the rat, GS Fraley, JM Scarlett, Shimada, I, DN Teklemichael, BV Acohido, DK Clifton, RA Steiner, DIABETES, 53, (5) 1237 - 1242,   2004年05月, 査読有り, Galanin-like peptide (GALP) is produced in a small population of neurons in the arcuate nucleus of the hypothalamus, and leptin stimulates the hypothalamic expression of GALP mRNA. Because insulin and leptin share common signaling pathways in the brain, we reasoned that GALP neurons might also be responsive to changes in circulating concentrations of insulin. To test this hypothesis, we first studied the effect of insulin deficiency on the expression of GALP by comparing levels of GALP mRNA between normal and diabetic animals. Streptozotocin-induced diabetes was associated with a significant reduction in the expression of GALP mRNA, which was reversed by treatment with either insulin or leptin. Second, we examined the effect of insulin administered directly into the brain on the expression of GALP mRNA in fasted rats. Hypothalamic levels of GALP mRNA were lower in animals after a 48-h fast, and central treatment with insulin reversed this effect. These results suggest that GALP neurons are direct targets for regulation by insulin and implicate these cells for a role in the metabolic and behavioural sequelae of type 1 diabetes.
  • Structure, expression, and cluster organization of genes encoding gonadotropin-releasing hormone receptors found in the neural complex of the ascidian Ciona intestinalis, T Kusakabe, S Mishima, Shimada, I, Y Kitajima, M Tsuda, GENE, 322, 77 - 84,   2003年12月, 査読有り, Gonadotropin-releasing hormone (GnRH) controls reproductive functions in vertebrates. In the present study, two distinct homologues (Ci-GnRER1 and Ci-GnRHR2) of the vertebrate GnRH receptor (GnRHR) were identified by cDNA cloning from the neural complex of the ascidian Ciona intestinalis. The Ci-GnRHR1 and Ci-GnRHR2 genes are closely linked to each other and form a cluster with another GnRHR-like gene in the genome. Ci-GnRBR1 and Ci-GnRHR2 are more closely related to vertebrate GnRHRs than to the GnRHR-related protein of Drosophila. The phylogenetic analysis indicates that vertebrates and urochordates independently acquired multiple GnRHRs by gene duplications that occurred during the evolution of each lineage. A voltage clamp of Xenopus oocytes injected with synthetic Ci-GnRHR1 mRNA revealed inward currents in response to an ascidian form of GnRB, suggesting that Ci-GnRHR1 is a bona-fide GnRHR. Expression patterns of Ci-GnKHR and Ci-GnRHR2 suggest that a GnRH signaling system is involved in regulation of neuronal and reproductive processes as well as in other physiological functions in ascidians. (C) 2003 Elsevier B.V. All rights reserved.
  • Differential patterns of Fos induction in the hypothalamus of the rat following central injections of galanin-like peptide and galanin, GS Fraley, Shimada, I, JW Baumgartner, RA Steiner, ENDOCRINOLOGY, 144, (4) 1143 - 1146,   2003年04月, 査読有り, Galanin and its newly discovered relative galanin-like peptide (GALP) are neuropeptides that are implicated in the neuroendocrine regulation of body weight and reproduction. GALP has been shown to bind in vitro to galanin receptor subtypes 1 and 2, but whether it has its own specific receptor(s) is unknown. We reasoned that if GALP acts through a receptor that is distinct from galanin receptors, then GALP should activate central pathways that are different from those activated by galanin. The purpose of this study was to determine whether galanin and GALP produce different patterns of neuronal activation within the hypothalamus. Quantitative analysis of Fos immunoreactivity showed that galanin induced a significantly greater number of Fos-positive nuclei in the paraventricular nucleus compared with GALP (P < 0.001); however, compared with galanin, GALP induced significantly more Fos-positive cells in the horizontal limb of the diagonal band of Broca, caudal preoptic area, arcuate nucleus, and median eminence (P < 0.05). These observations suggest that GALP and galanin act through different receptor-mediated pathways to exert their effects on the regulation of body weight and reproduction and identify target cells for GALP's specific actions in the hypothalamus, including the preoptic area, paraventricular and arcuate nuclei, and the median eminence.

受賞

  •   2010年11月, 北米神経科学会, ポスドクトラベルアワード
  •   2010年09月, アメリカ心臓協会, ポスドク生奨学金
  •   2009年12月, 北米神経科学会バーモントチャプター, ポスターアワード
  •   2009年11月, 北米神経科学会, 大学院生トラベルアワード
  •   2009年09月, アメリカ心臓協会, 大学院生奨学金
  •   2002年04月, 兵庫県・アジア太平洋間ネットワーク, 交換留学奨学金

教育活動情報

担当経験のある科目

  • 発展研究特別講義1(英語講義)Cilia, 名古屋市立大学
  • 生化学学生実習, 名古屋市立大学


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