詳細

森山　隆太郎 （モリヤマ　リュウタロウ）

  • 理工学部 生命科学科　准教授
Last Updated :2024/04/23

コミュニケーション情報 byコメンテータガイド

  • コメント

    生殖機能を制御するメカニズムについて研究しています。特に、脳・下垂体レベルでの制御メカニズム、栄養と生殖の関係、ストレスと生殖の関係、受精における精子の役割などに焦点を当てています。

研究者情報

学位

  • 博士（農学）名古屋大学

ホームページURL

J-Global ID

研究キーワード

  • 精巣   性腺刺激ホルモン   性腺刺激ホルモン放出ホルモン   長鎖脂肪酸   栄養   下垂体   精子   ホルモン   神経内分泌学   動物生理学・繁殖学   Animal Physiology and Reproduction   

現在の研究分野（キーワード）

    生殖機能を制御するメカニズムについて研究しています。特に、脳・下垂体レベルでの制御メカニズム、栄養と生殖の関係、ストレスと生殖の関係、受精における精子の役割などに焦点を当てています。

研究分野

  • ライフサイエンス / 動物生産科学
  • ライフサイエンス / 動物生理化学、生理学、行動学

経歴

  • 2011年04月 - 現在  近畿大学 理工学部Faculty of Science and Engineering講師
  • 2011年09月 - 2012年09月  ワシントン大学医学部産婦人科客員研究員
  • 2007年04月 - 2011年03月  近畿大学 理工学部Faculty of Science and Engineering助教
  • 2005年04月 - 2007年03月  近畿大学 理工学部Faculty of Science and Engineering助手
  • 2003年04月 - 2005年03月  農業生物資源研究所 非常勤職員

学歴

  •         - 2003年   名古屋大学   生命農学研究科   応用分子生命科学専攻
  •         - 1998年   名古屋大学   生命農学研究科 応用分子生命科学専攻
  •         - 1996年   明治大学   農学部   農学科

所属学協会

  • 日本下垂体研究会   Society for the Study of Reproduction   Society for Neuroscience   The Endocrine Society   日本神経科学会   日本比較内分泌学会   日本繁殖生物学会   日本畜産学会   日本内分泌学会   

研究活動情報

論文

  • Ryutaro Moriyama; Nobuyuki Fukushima
    Neuroscience letters 741 135506 - 135506 2021年01月 [査読有り]
     
    Lysophosphatidic acid receptor 1 (LPA1) is a receptor of lysophosphatidic acid (LPA). The present study investigated Lpar1 mRNA expression in the mouse pituitary gland by RT-PCR, in situ hybridization, and immunohistochemistry. Lpar1 mRNA was abundantly expressed in the pituitary gland. In situ hybridization and immunohistochemistry revealed over 90 % of a common glycoprotein α-subunit, luteinizing hormone β-subunit, and thyroid-stimulating hormone β-subunit immunoreactive cells co-expressed Lpar1 mRNA in the anterior pituitary gland, but few growth hormone, adrenocorticotropic hormone, and prolactin cells co-expressed Lpar1. Furthermore, Lpar1 mRNA levels in the pituitary gland were increased after ovariectomy and decreased after E2 administration. These results demonstrate that LPA1-mediated signaling may play physiological roles in gonadotropes and thyrotropes in the mouse pituitary gland.
  • Chikaya Deura; Yusuke Kimura; Takumi Nonoyama; Ryutaro Moriyama
    The Journal of reproduction and development 66 3 249 - 254 2020年06月 [査読有り]
     
    GPR120 is a long-chain fatty acid (LCFA) receptor that is specifically expressed in gonadotropes in the anterior pituitary gland in mice. The aim of this study was to investigate whether GPR120 is activated by free fatty acids in the pituitary of mice and mouse immortalized gonadotrope LβT2 cells. First, the effects of palmitate on GPR120, gonadotropic hormone b-subunits, and GnRH-receptor expression in gonadotropes were investigated in vitro. We observed palmitate-induced an increase in Gpr120 mRNA expression and a decrease in follicle-stimulating hormone b-subunit (Fshb) expression in LβT2 cells. Furthermore, palmitate exposure caused the phosphorylation of ERK1/2 in LβT2 cells, but no significant changes were observed in the expression levels of luteinizing hormone b-subunit (Lhb) and gonadotropin releasing hormone-receptor (Gnrh-r) mRNA and number of GPR120 immunoreactive cells. Next, diurnal variation in Gpr120 mRNA expression in the male mouse pituitary gland was investigated using ad libitum and night-time restricted feeding (active phase from 1900 to 0700 h) treatments. In ad libitum feeding group mice, Gpr120 mRNA expression at 1700 h was transiently higher than that measured at other times, and the peak blood non-esterified fatty acid (NEFA) levels were observed from 1300 to 1500 h. These results were not observed in night-time-restricted feeding group mice. These results suggest that GPR120 is activated by LCFAs to regulate follicle stimulating hormone (FSH) synthesis in the mouse gonadotropes.
  • Sho Nakamura; Kohei Noda; Masafumi Miwa; Shiori Minabe; Teruki Hagiwara; Akira Hirasawa; Shuichi Matsuyama; Ryutaro Moriyama
    The Journal of reproduction and development 66 2 135 - 141 2020年04月 [査読有り]
     
    Negative energy balance in domestic animals suppresses their reproductive function. These animals commonly use long-chain fatty acids (LCFAs) from adipocytes as an energy source under states of malnutrition. The G-protein coupled receptor, GPR120, is a specific receptor for LCFAs, but its role in reproductive function remains unknown in domestic animals. The purpose of this study was to examine whether GPR120 is involved in the reproductive system of cattle. GPR120 mRNA expression was evaluated in brain, pituitary, and ovarian tissue samples by RT-PCR. GPR120 gene expression was detected with high intensity only in the anterior pituitary sample, and GPR120-immunoreactive cells were found in the anterior pituitary gland. Double immunohistochemistry of GPR120 in the anterior pituitary hormone-producing cells, such as gonadotropes, thyrotropes, lactotropes, somatotropes, and corticotropes, was performed to clarify the distribution of GPR120 in the anterior pituitary gland of ovariectomized heifers. Luteinizing hormone β subunit (LHβ)- and follicle-stimulating hormone β subunit (FSHβ)-immunoreactive cells demonstrated GPR120 immunoreactivity at 80.7% and 85.9%, respectively. Thyrotropes, lactotropes, somatotropes, and corticotropes coexpressed GPR120 at 21.1%, 5.4%, 13.6%, and 14.5%, respectively. In conclusion, the present study suggests that GPR120 in the anterior pituitary gland might mediate LCFA signaling to regulate gonadotrope functions, such as hormone secretion or production, in cattle.
  • Chikaya Deura; Ryutaro Moriyama
    The Journal of reproduction and development 66 2 143 - 148 2020年04月 [査読有り]
     
    High-fat diet (HFD) is associated with the regulation of reproductive functions. This study aimed to investigate the effects of short-term HFD on the mRNA expression levels of follicle-stimulating hormone β subunit (FSHβ), luteinizing hormone β subunit (LHβ), gonadotropin-releasing hormone receptor, and long-chain fatty acid receptor, GPR120, in the matured male mouse pituitary gland. Adult male mice were fed either control chow or HFD for 1, 2, 5, 10, 30 and 150 days. Fshb and Gpr120 mRNA expression levels in the pituitary glands were significantly increased during 2 to 30 days of HFD feeding. Gnrh-r mRNA in the 30 days HFD fed group and body weight in the 30 and 150 days HFD fed groups were higher than control. However, there were no significant differences in plasma non-esterified fatty acids or glucose levels during the 150 days of HFD feeding. These results suggest that male mice feeding a short-term HFD induces FSHβ synthesis and GPR120 expression in their pituitary gonadotropes.
  • Moriyama R; Iwamoto K; Hagiwara T; Yoshida S; Kato T; Kato Y
    The Journal of reproduction and development 66 2 97 - 104 2020年04月 [査読有り]
     
    Malnutrition is one of the factors that induces reproductive disorders. However, the underlying biological processes are unclear. AMP-activated protein kinase (AMPK) is an enzyme that plays crucial role as a cellular energy sensor. In the present study, we examined the effects of AMPK activation on the transcription of the murine gonadotropin subunit genes Cga, Lhb, and Fshb, and the gonadotropin-releasing hormone receptor Gnrh-r. Real-time PCR and transcription assay using LβT2 cells demonstrated that 5-amino-imidazole carboxamide riboside (AICAR), a cell-permeable AMP analog, repressed the expression of Lhb. Next, we examined deletion mutants of the upstream region of Lhb and found that the upstream regulatory region of Lhb (-2527 to -2198 b) was responsible for the repression by AICAR. Furthermore, putative transcription factors (SP1, STAT5a, and TEF) that might mediate transcriptional control of the Lhb repression induced by AICAR were identified. In addition, it was confirmed that both AICAR and a competitive inhibitor of glucose metabolism, 2-deoxy-D-glucose, induced AMPK phosphorylation in LβT2 cells. Therefore, the upstream region of Lhb is one of the target sites for glucoprivation inducing AMPK activation. In addition, AMPK plays a role in repressing Lhb expression through the distal -2527 to -2198 b region.
  • Ryutaro Moriyama; Kaho Ueda; Chikaya Deura
    Endocrine journal 64 11 1055 - 1061 2017年11月 [査読有り]
     
    GPR120 is a G-protein-coupled receptor that is activated by long-chain fatty acids. In our previous study, GPR120 expression was detected in gonadotrophs of the mouse anterior pituitary gland. It is well known that the function of anterior pituitary cells is largely under the influence of circulating sex steroids. Thus, in the present study, we investigated the modulatory roles of the ovarian hormones, estrogen (E2) and progesterone (P), on the expression levels of GPR120 mRNA in mouse pituitary glands. GPR120 mRNA expression levels in the pituitary gland were increased after ovariectomy or P treatment, and were decreased after the administration of E2. Simultaneous injection of E2 and P interfered with the action of E2 on GPR120 mRNA expression. The GnRH antagonist, Cetrotide, did not inhibit the increase in GPR120 expression in ovariectomized (OVX) animals. In addition, immunohistochemistry revealed that more than 95.4% of GPR120 immunoreactive cells colocalized with the luteinizing hormone β (LHβ) in the anterior pituitary gland of intact, ovariectomized (OVX), estradiol-primed OVX (OVX+E2), or progesterone-primed OVX (OVX+P) animals. Furthermore, GPR120 mRNA expression levels were not significantly different in the pituitary gland of females throughout the ovarian cycle. It is suggested that low levels of P may mask the inhibitory effect of estradiol on the synthesis of GPR120 in the estrous stage in intact animals. These results demonstrate that ovarian hormones may directly regulate GPR120 expression in the reproductive cycle at the pituitary level.
  • Moriyama R; Yamazaki T; Kato T; Kato Y
    The Journal of reproduction and development 62 2 195 - 9 2016年04月 [査読有り]
     
    Here, we assessed the effects of long-chain fatty acids (LCFAs) and the LCFA receptor agonist GW9508 on the transcription of the gonadotropin subunit genes Cga, Lhb and Fshb because LCFA receptor GPR120 was observed in mouse gonadotropes in our recent study. A transcription assay using LβT2 cells demonstrated that LCFAs, oleic acid, α-linolenic acid, docosahexaenoic acid and palmitate, repressed the expression of Cga, Lhb, and Fshb at concentrations between 50 and 100 µM. On the other hand, treatment with 10 µM unsaturated LCFAs, oleic acid, α-linolenic acid and docosahexaenoic acid, repressed only Fshb expression, while the same dose of a saturated LCFA, palmitate, had no effect on the expression of gonadotropin subunit genes. Furthermore, GW9508 did not affect promoter activity. Next, we examined deletion mutants of the upstream region of Fshb and found that the upstream regulatory region (-2824 to -2343 bp) of Fshb was responsible for the notable repression by 10 µM unsaturated LCFAs. Our results suggest that the upstream region of Fshb is susceptible to unsaturated LCFAs. In addition, unsaturated LCFAs play a role in repressing Fshb expression through the distal -2824 to -2343 bp region, which might be independent of the LCFA receptor GPR120 pathway.
  • Ryutaro Moriyama; Chikaya Deura; Shingo Imoto; Kazuhiro Nose; Nobuyuki Fukushima
    Histochemistry and cell biology 143 1 21 - 7 2015年01月 [査読有り]
     
    G-protein-coupled receptor 120 (GPR120) has been known to be a receptor of long-chain fatty acids. Here, we investigated GPR120 expression in the mouse pituitary gland via real-time PCR, in situ hybridization, and immunohistochemistry. GPR120 mRNA was abundantly expressed in the pituitary gland of ad-lib fed animals. In situ hybridization and immunohistochemistry revealed GPR120 expression in the gonadotropes of the anterior pituitary gland, but not in thyrotropes, somatotropes, lactotropes, corticotropes, melanotropes, and the posterior pituitary gland. Furthermore, 24 h of fasting induced an increase in GPR120 mRNA expression in the pituitary gland. These results demonstrate that GPR120 in mouse pituitary gonadotropes is upregulated by fasting and that it may play a role in controlling gonadotropin secretion.
  • Simina M Popa; Ryutaro M Moriyama; Claudia S Caligioni; Jasmine J Yang; Caroline M Cho; Tessa L Concepcion; Amy E Oakley; In Hae Lee; Elisenda Sanz; Paul S Amieux; Alain Caraty; Richard D Palmiter; Victor M Navarro; Yee-Ming Chan; Stephanie B Seminara; Donald K Clifton; Robert A Steiner
    Endocrinology 154 8 2784 - 94 2013年08月 [査読有り]
     
    Kisspeptin (Kiss1) signaling to GnRH neurons is widely acknowledged to be a prerequisite for puberty and reproduction. Animals lacking functional genes for either kisspeptin or its receptor exhibit low gonadotropin secretion and infertility. Paradoxically, a recent study reported that genetic ablation of nearly all Kiss1-expressing neurons (Kiss1 neurons) does not impair reproduction, arguing that neither Kiss1 neurons nor their products are essential for sexual maturation. We posited that only minute quantities of kisspeptin are sufficient to support reproduction. If this were the case, animals having dramatically reduced Kiss1 expression might retain fertility, testifying to the redundancy of Kiss1 neurons and their products. To test this hypothesis and to determine whether males and females differ in the required amount of kisspeptin needed for reproduction, we used a mouse (Kiss1-CreGFP) that has a severe reduction in Kiss1 expression. Mice that are heterozygous and homozygous for this allele (Kiss1(Cre/+) and Kiss1(Cre/Cre)) have ∼50% and 95% reductions in Kiss1 transcript, respectively. We found that although male Kiss1(Cre/Cre) mice sire normal-sized litters, female Kiss1(Cre/Cre) mice exhibit significantly impaired fertility and ovulation. These observations suggest that males require only 5% of normal Kiss1 expression to be reproductively competent, whereas females require higher levels for reproductive success.
  • Daisuke Furuta; Masayuki Yamane; Toshifumi Tsujiuchi; Ryutaro Moriyama; Nobuyuki Fukushima
    Molecular and cellular neurosciences 50 1 21 - 34 2012年05月 [査読有り]
     
    Although neurite branching is crucial for neuronal network formation after birth, its underlying mechanisms remain unclear. Here, we demonstrate that lysophosphatidic acid (LPA) stimulates neurite branching through a novel signaling pathway. Treatment of neuronal cell lines with LPA resulted in neurite branch formation when LPA(3) receptor was introduced. The effects of LPA were blocked by inhibition of G(q) signaling. Furthermore, expression of inhibitory mutants of the small GTPase Rnd2/Rho7 or an Rnd2 effector rapostlin abolished LPA(3)-mediated neurite branching. The LPA(3) agonist 2(S)-OMPT or LPA also induced axonal branch formation in hippocampal neurons, which was blocked by G(q) and Rnd2 pathway inhibition or LPA(3) knockdown. These findings suggest that the novel signaling pathway involving LPA(3), G(q), and Rnd2 may play an important role in neuronal network formation.
  • Analytical study of interaction between spdider toxin and glutamate receptors.
    T. Nishimaru; R. Moriyama; T. Wada; S. Yoshida; K. Shimamoto; M. Nishizawa; S. Ito; Y. Yamaguchi; T. Wakamiya
    Peptide Science 2009 349 - 352 2010年 [査読有り]
  • Nobuyuki Fukushima; Daisuke Furuta; Yuji Hidaka; Ryutaro Moriyama; Toshifumi Tsujiuchi
    Journal of neurochemistry 109 3 683 - 93 2009年05月 [査読有り]
     
    Many studies have shown that microtubules (MTs) interact with MT-associated proteins and motor proteins. These interactions are essential for the formation and maintenance of the polarized morphology of neurons and have been proposed to be regulated in part by highly diverse, unusual post-translational modifications (PTMs) of tubulin, including acetylation, tyrosination, detyrosination, Delta2 modification, polyglutamylation, polyglycylation, palmitoylation, and phosphorylation. However, the precise mechanisms of PTM generation and the properties of modified MTs have been poorly understood until recently. Recent PTM research has uncovered the enzymes mediating tubulin PTMs and provided new insights into the regulation of MT-based functions. The identification of tubulin deacetylase and discovery of its specific inhibitors have paved the way to understand the roles of acetylated MTs in kinesin-mediated axonal transport and neurodegenerative diseases such as Huntington's disease. Studies with tubulin tyrosine ligase (TTL)-null mice have shown that tyrosinated MTs are essential in normal brain development. The discovery of TTL-like genes encoding polyglutamylase has led to the finding that polyglutamylated MTs which accumulate during brain development are involved in synapse vesicle transport or neurite outgrowth through interactions with motor proteins or MT-associated proteins, respectively. Here we review current exciting topics that are expected to advance MT research in the nervous system.
  • Study directed toward the analysis of interaction between the spider toxin NPTX-594 and glutamate receptors.
    T. Nishimaru; R. Moriyama; T. Wada; S. Yoshida; K. Shimamoto; M. Nishizawa; S. Ito; Y. Yamaguchi; T. Wakamiya
    Peptide Science 2008 401 - 404 2009年 [査読有り]
  • D. Furuta; R. Moriyama; N. Fukushima
    Science and Technology 21 21 19 - 23 近畿大学理工学総合研究所 2009年 
    Green fluorescent protein (GFP)-tagged tubulin has been widely employed to examine tubulin dynamics in living cells. In the present study, we biochemically re-evaluate the property of GFP-tubulin expressed in cells. When expressed in mammalian cells, antibodies against GFP or the amino-terminal region of tubulin detected GFP-tubulin in western blot analyses. By contrast, antibodies against the carboxyl terminal region of tubulin failed to recognize exogenous GFP-tubulin, but not endogenous tubulin. These results indicate that GFP-tubulin is partially truncated at the carboxyl terminal region and suggest that data of experiments using GFP-tubulin should be carefully analyzed.
  • Shinya Shano; Kazuki Hatanaka; Shinsuke Ninose; Ryutaro Moriyama; Toshifumi Tsujiuchi; Nobuyuki Fukushima
    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 1783 5 748 - 759 2008年05月 [査読有り]
     
    Lysophosphatidic acid (LPA) is an extracellular signaling lipid that regulates cell proliferation, survival, and motility of normal and cancer cells. These effects are produced through G protein-coupled LPA receptors, LPA(1) to LPA(5). We generated an LPA(1) mutant lacking the SerValVal sequence of the C-terminal PDZ-binding domain to examine the role of this domain in intracellular signaling and other cellular functions. B103 neuroblastoma cells expressing the mutant LPA(1) showed rapid cell proliferation and tended to form colonies under serum-free conditions. The enhanced cell proliferation of the mutant cells was inhibited by exogenous expression of the plasmids inhibiting G proteins including G(beta gamma), G(alpha i) and G(alpha q) or G(alpha 12/13), or treatment with pertussis toxin, phosphoinositide 3-kinase (PI3K) inhibitors or a Rho inhibitor. We confirmed that the PI3K-Akt and Rho pathways were intrinsically activated in mutant cells by detecting increases in phosphorylated Akt in western blot analyses or by directly measuring Rho activity. Interestingly, expression of the mutant LPA(1) in non-tumor mouse fibroblasts induced colony formation in a clonogenic soft agar assay, indicating that oncogenic pathways were activated. Taken together, these observations suggest that the mutant LPA(1) constitutively activates the G protein signaling leading to PI3K-Akt and Rho pathways, resulting in enhanced cell proliferation. (C) 2007 Elsevier B.V. All rights reserved.
  • Shinya Shano; Ryutaro Moriyama; Jerold Chun; Nobuyuki Fukushima
    Neurochemistry international 52 1-2 216 - 20 2008年01月 [査読有り]
     
    Lysophosphatidic acid (LPA) is an extracellular lipid mediator that regulates nervous system development and functions through multiple types of LPA receptors. Here we explore the role of LPA receptor subtypes in cortical astrocyte functions. Astrocytes cultured under serum-free conditions were found to express the genes of five LPA receptor subtypes, lpa1 to lpa5. When astrocytes were treated with dibutyryl cyclic adenosine monophosphate, a reagent inducing astrocyte differentiation or activation, lpa1 expression levels remained unchanged, but those of other LPA receptor subtypes were relatively reduced. LPA stimulated DNA synthesis in both undifferentiated and differentiated astrocytes, but failed to do so in astrocytes prepared from mice lacking lpa1 gene. LPA also inhibited [3H]-glutamate uptake in both undifferentiated and differentiated astrocytes; and LPA-induced inhibition of glutamate uptake was still observed in lpa1-deficient astrocytes. Taken together, these observations demonstrate that LPA1 mediates LPA-induced stimulation of cell proliferation but not inhibition of glutamate uptake in astrocytes.
  • Nobuyuki Fukushima; Shinya Shano; Ryutaro Moriyama; Jerold Chun
    Neurochemistry international 50 2 302 - 7 2007年01月 [査読有り]
     
    Lysophosphatidic acid (LPA) is an extracellular lipid mediator that regulates cortical development. Here we examined how LPA influences the cell fate of cortical neuroblasts using a neurosphere culture system. We generated neurospheres in the presence of basic fibroblast growth factor (bFGF). Treatment with LPA throughout the culture period significantly reduced the number of cells in the neurospheres. When dissociated single cells derived from neurospheres were induced to differentiate by adherence on coverslips, the proportion of MAP2-positive neurons was higher in LPA-treated neurospheres than in those treated with bFGF alone, and the proportion of myelin basic protein-positive oligodendrocytes was lower. Consistent with this finding, LPA raised the ratio of beta-tubulin type III-positive young neurons and reduced the ratio of CD140a-positive oligodendrocyte precursors in neurospheres. These effects of LPA were inhibited by pretreatment of neurospheres with pertussis toxin or an LPA(1)-preferring antagonist, Ki16425. Moreover, LPA-induced enhancement of neuronal differentiation was not observed in neurospheres derived from lpa(1)-null mice. These results suggest that LPA promotes the commitment of neuroblasts to the neural lineage through the LPA(1)-G(i/o) pathway.
  • 伊藤 秀一; 矢用 健一; 松山 秀一; 森山 隆太郎; 須藤 まどか; 粕谷 悦子; 大蔵 聡; 岡村 裕昭
    日本家畜管理学会誌・応用動物行動学会誌 42 4 203 - 208 日本家畜管理学会 2006年 [査読有り]
     
    ホルスタイン種牛における隔離ストレス反応の緩和を目的として、社会的隔離環境に暴露したホルスタイン種去勢牛に、既知個体または供試個体自身の映像を提示して、行動反応および生理反応に与える影響を調査した。供試牛4頭に頸静脈カテーテルを装着し、スタンチョン式の実験室での飼育に馴致した。実験では、他の3頭を実験室から出すことで、対象牛1頭を実験室に残して、社会的隔離環境とした。他の個体を退出させると同時に、ほぼ原寸大の既知個体の映像、または供試個体自身の映像を供試牛の正面約1.5mに設置したスクリーンに、液晶プロジェクターを用いて提示した。対照区の映像は、ブルーバックのみとした。隔離環境に暴露してから0,30,60,90,120,150,180分後に採血を行った。また、採食行動、反芻行動、立位休息、伏臥位休息、立位不動化に費やす時間と、発声回数を記録した。隔離環境に暴露しない状態と、隔離してブルーバックのみの提示とを比較したところ、後者では採食、伏臥位休息、反芻行動の減少傾向(P=0.068)がみられ、立位休息および発声回数が増加する傾向となった(P=0.068)。血中コルチゾル濃度およびACTH濃度に有意な上昇は認められなかった。隔離ストレス負荷時に、映像を提示しない場合は、反芻行動に費やす割合は16.9±6.1%であったが、既知の他個体の動画を映写することによって、反芻に費やす割合が36.0±3.3%と増加する傾向がみられた(P=0.068)。供試牛自身の映像による隔離ストレス緩和の効果は認められなかった。本研究から、隔離ストレスを負荷したホルスタイン種牛に対して、同種他個体の映像を提示することは、反芻行動に費やす時間を増加させることなど、ストレス反応の一部緩和につながる可能性が示唆された。
  • Ryutaro Moriyama; Hiroko Tsukamura; Mika Kinoshita; Hirokatsu Okazaki; Yukio Kato; Kei-Ichiro Maeda
    Endocrinology 145 5 2507 - 15 2004年05月 [査読有り]
     
    Pancreatic glucokinase (GK)-like immunoreactivities are located in ependymocytes and serotonergic neurons of the rat brain. The present study investigated in vitro changes in intracellular calcium concentrations ([Ca(2+)](i)) in response to low (2 mm) or high (20 mm) extracellular glucose concentrations in isolated cells from the wall of the central canal (CC), raphe obscurus nucleus (ROb), ventromedial hypothalamus (VMH), and lateral hypothalamic area (LHA) in male rats. An increase in [Ca(2+)](i) was found in cells from the CC (21.1% or 9.8% of ependymocytes), ROb (10.9% or 14.5% of serotonergic neurons), VMH (7.8% and 25.2% of neurons), and LHA (20% or 15.7% of neurons), when extracellular glucose levels were changed from 10 to either 2 or 20 mm, respectively. Most of the ependymocytes and serotonergic neurons responding to the glucose changes were immunoreactive to the anti-GK in the CC (96.8% for low glucose and 100% for high glucose) and ROb (100% for low and high glucose). The [Ca(2+)](i) increase was blocked with calcium-free medium or L-type calcium channel blocker. Cells with an increase in [Ca(2+)](i) in response to low glucose did not respond to high glucose and vice versa. Inhibition of GK activity with acute alloxan treatment blocked low or high glucose-induced [Ca(2+)](i) increases in most GK-immunoreactive cells from the CC or ROb. The glucose-sensitive [Ca(2+)](i) increase in neurons of the VMH and LHA was also alloxan-sensitive, but no cells taken from the VMH and LHA were immunoreactive to the antibody used. The present study further indicates that ependymocytes of the CC and serotonergic neurons in the ROb are also sensitive to the changes in extracellular glucose in a GK-dependent manner, but that the subtype of GK in these cells could be different from that in the VMH and LHA.
  • M Kinoshita; R Moriyama; H Tsukamura; KI Maeda
    DOMESTIC ANIMAL ENDOCRINOLOGY 25 1 109 - 120 2003年07月 [査読有り]
     
    Energy availability has been considered to regulate gonadal activity by modulating the release of gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) at various reproductive phases, such as lactation and puberty in domestic as well as wild animals. Experimental models with rats and sheep have demonstrated that fasting or glucoprivation suppresses pulsatile LH release. From those experiments, the information on energy deficiency is considered to be detected by specific central sensors and conveyed to the hypothalamus to regulate LH release as well as food intake. Noradrenergic neurons, originating in the medulla oblongata and projecting to the hypothalamic paraventricular nucleus (PVN), is reported to be one of the pathways mediating the response of LH release to energy deficiency. The other component is considered to be an energy-sensing mechanism in the brain. Glucose or other oxidizable fuels may function as a metabolic signal to regulate LH release. Previous studies suggest the presence of a glucose-sensing mechanism in the rat hindbrain. From our previous results in the rat, the ependymocytes lining the wall of the cerebroventricle could possibly serve as a glucose sensor to regulate GnRH/LH release. Greater understanding of the nature of the energy-sensing mechanism in the brain will contribute to the nutritional manipulation of reproductive performance in domestic animals in various conditions. (C) 2003 Elsevier Inc. All rights reserved.
  • Ryutaro Moriyama; Beverly A S Reyes; Hiroko Tsukamura; Kei-ichiro Maeda
    The Journal of reproduction and development 49 2 151 - 7 2003年04月 [査読有り]
     
    Glucoprivation induced by 2-deoxy-D-glucose (2DG) suppresses pulsatile luteinizing hormone (LH) secretion in female rats. The suppression is enhanced in the presence of estrogen. In the present study, 2DG-induced Fos expression was examined in the solitary tract nucleus (NTS), hypothalamic paraventricular nucleus (PVN), raphe obscurus nucleus (ROb) and raphe pallidus nucleus (RPa), which have been previously suggested to be involved in glucoprivation-induced suppression of LH secretion in female rats. Ovariectomized (OVX) or estrogen-primed ovariectomized (OVX+E(2)) rats were injected intravenously with 2DG (400 mg/kg BW). The brain was removed 1 h after the injection. The number of Fos-like-immunoreactive (Fos-li) cells in the PVN and NTS was significantly increased in OVX+E(2) rats compared with control groups, but did not show a significant increase in the OVX group. Few Fos-li cells were observed in the ROb and RPa in all groups. All of the Fos-li cells in the PVN and NTS were neurons because they had immunoreactivities to microtubule-associated protein 2. Some Fos-li cells (8.3%) had tyrosine hydroxylase-like immunoreactivities in the NTS in 2DG-treated OVX+E(2) rats. These results suggest that neurons in the PVN and NTS are involved in the estrogen-dependent neural cascade mediating glucoprivic suppression of LH secretion in female rats.
  • H Tsukamura; RC Thompson; S Tsukahara; S Ohkura; F Maekawa; R Moriyama; Y Niwa; DL Foster; KI Maeda
    JOURNAL OF NEUROENDOCRINOLOGY 12 6 529 - 534 2000年06月 [査読有り]
     
    Melanin-concentrating hormone (MCH) has been reported to be involved in the regulation of feeding behaviour in rats and mice. Because many neuropeptides that influence ingestive behaviour also regulate reproductive function, the present study was designed to determine if central administration of MCH changes pulsatile secretion of luteinizing hormone (LH) in the rats. Wistar-Imamichi strain female rats were ovariectomized and implanted with oestradiol to produce a moderate inhibitory feedback effect on LH release. The effects of i.c.v. injections of MCH on LH release were examined in freely moving animals. Blood samples were collected every 6 min for 3 h through an indwelling cannula. After 1 h of sampling, MCH (0.1, 1 or 10 mu g/animal) or vehicle (saline) was injected into the third cerebroventricle. Because MCH is also reported to affect the hypothalamo-pituitary-adrenal (HPA) axis, which in turn, can influence reproductive function, plasma corticosterone concentrations were determined in the same animals at 30-min intervals during the first and last hours and every 12 min during the second hour of the 3-h sampling period. When expressed as per cent changes, mean plasma LH concentrations after MCH administration were significantly tower in the animals injected with all doses of the peptide compared with vehicle-treated animals; LH pulse frequency was significantly lowered by 1 mu g of MCH. Per cent changes in mean plasma corticosterone levels were not significantly affected by MCH administration. These results in oestradiol-treated ovariectomized rats indicate that central MCH is capable of inhibiting pulsatile LH secretion. We have previously shown that 48-h fasting suppresses pulsatile LH release in the presence of oestrogen, Take together, these results raise the possibility that MCH could play a role in mediating the suppression of LH secretion during periods of reduced nutrition.
  • H Tsukamura; S Tsukahara; F Maekawa; R Moriyama; BAS Reyes; T Sakai; Y Niwa; DL Foster; KI Maeda
    JOURNAL OF NEUROENDOCRINOLOGY 12 5 403 - 408 2000年05月 [査読有り]
     
    Motilin is secreted in a clear episodic pattern during fasting or during the interdigestive phase, but feeding promptly stops this secretory pattern, and plasma concentrations of motilin decrease. We have previously determined that fasting markedly suppresses pulsatile luteinizing hormone (LH) secretion in female rats in the presence of oestrogen. In the present study, we wished to learn if motilin may mediate the fasting-induced suppression of LH secretion by determining the effects of motilin administration on LH release and on food intake. Intravenous (i.v.) injection of motilin (37 nmol/rat) suppressed LH release and significantly decreased mean LH concentrations both in ovariectomized (OVX) and oestradiol-implanted ovariectomized (OVX + E-2) rats. Food intake was significantly increased by i.v. motilin injection in OVX rats, but not in OVX + E-2 rats. It is likely that motilin inhibits LH release via inhibition of the gonadotrophin-releasing hormone (GnRH)-releasing mechanism at the hypothalamic level, because motilin (3.7 nmol/rat) also suppressed LH secretion when centrally administered, and because LH release in i.v. motilin-treated rats increased in response to exogenous GnRH. These results suggest that motilin may be a peripheral signal for the suppression of LH secretion through central sensors.
  • Neuroendocrine aspects of nutritional regulation of the gonadal axis: concepts derived from the rat model.
    K. -I. Maeda; F.R.A. Cagampang; S. Nagatani; M.A.C. Estacio; K. Murahashi; R. Moriyama; A. Kuroda; S. Tsukahara; D.C. Bucholtz; R. Thompson; D.L. Foster; H. Tsukamura
    Reproductive biology update 271 - 279 1998年

講演・口頭発表等

  • Molecular mechanism of LPA3-mediated axonal branching formation in cultured hippocampal neurons  [通常講演]
    古田大祐; 山根昌之; 森山 隆太郎; 辻内俊文; 福嶋 伸之; 立命館大学薬学部
    第83回生化学会大会 2010年12月 神戸 第83回生化学会大会
  • Lysophosphatidic acid receptor 3 activation induces axonal branch formation in cultured hippocampal neurons  [通常講演]
    福嶋 伸之; 古田大祐; 山根昌之; 辻内俊文; 森山 隆太郎
    Neuro2010 （第33回神経科学会、第53回神経化学会） 2010年09月 神戸 Neuro2010 （第33回神経科学会、第53回神経化学会）
  • 長鎖脂肪酸はマウス下垂体のGpr120 mRNA発現量を増加させる.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第25回下垂体研究会学術集会 2010年08月 伊良湖、伊良湖ガーデンホテル 第25回下垂体研究会学術集会
  • Long-chain fatty acids regulate GnRH receptor mRNA expression level in the gonadotrope of the mouse anterior pituitary gland.  [通常講演]
    森山 隆太郎; 福嶋伸之
    43rd Annual Meeting of the Society for the Study of Reproduction 2010年08月 Milwaukee, Wisconsin, U.S.A. 43rd Annual Meeting of the Society for the Study of Reproduction
  • クモ毒NPTX-594のCa2+透過性グルタミン酸受容体に対する阻害効果について  [通常講演]
    和田 哲幸; 市田 成志; 船上 仁範; 若宮 建昭; 吉田 繁; 森山 隆太郎
    日本薬学会 第130年会 2010年03月 日本薬学会 第130年会
  • Palmitate regulates GnRH receptor mRNA expression level in the gonadotrope of the mouse anterior pituitary gland.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    14th International Congress of Endocrinology 2010年03月 kyoto 14th International Congress of Endocrinology
  • 2-deoxy-D-glucose (2DG) induced glucoprivation suppressed gonadotropin-releasing hormone receptor (GnRH-R) and follicular stimulating hormone β subunit (FSHβ) mRNA expression levels in the LβT2 gonadotroph cells.  [通常講演]
    森山 隆太郎; 福嶋伸之
    14th International Congress of Endocrinology 2010年03月 Kyoto 14th International Congress of Endocrinology
  • グルコースの利用阻害は下垂体の性腺刺激ホルモン産生細胞でGnRHレセプターおよびFSHβ mRNA発現量を抑制する.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第102回日本繁殖生物学会大会 2010年 奈良、近畿大学 第102回日本繁殖生物学会大会
  • Lysophosphatidic acid receptor 3 is involved in neurite branching formation in hippocampal neurons  [通常講演]
    古田大祐; 山根昌之; 森山 隆太郎; 辻内俊文; 福嶋 伸之
    第82回日本生化学会大会 2009年10月 神戸 第82回日本生化学会大会
  • 高脂肪食負荷がゴナドトロフの長鎖脂肪酸受容体Gpr120と性腺刺激ホルモンmRNA発現に与える影響.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第102回日本繁殖生物学会大会 2009年09月 奈良、近畿大学 第102回日本繁殖生物学会大会
  • 高脂肪食給餌が成熟雄マウス下垂体のゴナドトロフに局在する長鎖脂肪酸受容体GPR120と性腺刺激ホルモンmRNA発現に与える影響.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第24回下垂体研究会学術集会 2009年08月 三沢、小牧温泉 青森屋 第24回下垂体研究会学術集会
  • グルコースの利用阻害はゴナドトロフ株化細胞LβT2で性腺刺激ホルモン放出ホルモン受容体 (GnRH-R) と卵胞刺激ホルモンβ鎖 (FSHβ) mRNA発現量を抑制する.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第24回下垂体研究会学術集会 2009年08月 三沢、小牧温泉 青森屋 第24回下垂体研究会学術集会
  • LPA induces neurite shape changes through LPA3  [通常講演]
    古田大祐; 山根昌之; 森山 隆太郎; 辻内俊文; 福嶋 伸之
    PLM2009 2009年05月 Tokyo PLM2009
  • Palmitate regulates GnRH receptor mRNA expression level in the gonadotrope of the mouse pituitary gland.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第5回武田科学振興財団薬科学シンポジウム 2009年05月 東京、グランドプリンスホテル高輪 第5回武田科学振興財団薬科学シンポジウム
  • LPA1 mRNA expression level in mouse pituitary gonadotropes is enhanced by ovariectomy.  [通常講演]
    森山 隆太郎; 福嶋伸之; 吉田 繁
    4th International Conference on Phospholipase A2 and Lipid Mediators 2009年05月 Tokyo 4th International Conference on Phospholipase A2 and Lipid Mediators
  • マウス下垂体のリゾホスファチジン酸受容体1はエストロジェン依存的に発現が抑制される.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第101回日本繁殖生物学会大会 2008年09月 福岡、九州大学 第101回日本繁殖生物学会大会
  • 森山 隆太郎; 福嶋 伸之
    第35回 日本神経内分泌学会・第23 回日本下垂体研究会合同学術集会 2008年08月 東京、政策研究大学院大学 第35回 日本神経内分泌学会・第23 回日本下垂体研究会合同学術集会
  • Palmitate regulates GnRH receptor mRNA expression in the gonadotrope of the mouse anterior pituitary  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第31回日本神経科学大会 2008年07月 東京、東京国際フォーラム 第31回日本神経科学大会
  • Fasting induced increase in long-chain fatty acid receptor GPR120 expression in the gonadotrope of the mouse anterior pituitary.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    37th Annual Meeting of Society for Neuroscience 2007年11月 San Diego, U. S. A. 37th Annual Meeting of Society for Neuroscience
  • グルコースと長鎖脂肪酸の濃度変化はマウス下垂体前葉のゴナドトロフで長鎖脂肪酸受容体GPR120 mRNA発現量を制御する.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第100回日本繁殖生物学会大会 2007年10月 東京、東京大学 第100回日本繁殖生物学会大会
  • Palmitate-induced increase in long-chain fatty acid receptor GPR120 mRNA level in LβT2 pituitary gonadotrope cells.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第30回日本神経科学大会 2007年09月 横浜、パシフィコ横浜 第30回日本神経科学大会
  • マウスのゴナドトロフで長鎖脂肪酸受容体GPR120 mRNA発現量を制御する因子の検討  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第22回下垂体研究会学術集会 2007年08月 葉山、湘南国際村センター 第22回下垂体研究会学術集会
  • マウスのゴナドトロフに発現する長鎖脂肪酸受容体GPR120.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第99回日本繁殖生物学会大会 2006年09月 名古屋、名古屋大学 第99回日本繁殖生物学会大会
  • Fasting induced Long-chain fatty acid receptor GPR120 expression increase in the anterior pituitary of mouse.  [通常講演]
    森山 隆太郎; 福嶋 伸之
    第29回日本神経科学大会 2006年07月 京都、国立京都国際会館 第29回日本神経科学大会

MISC

受賞

  • Journal of Reproduction and Development Outstanding Paper Award in 2003
     JPN
  • 第23回日本下垂体研究会学術集会特別優秀発表賞 (2008年度)

共同研究・競争的資金等の研究課題

  • 日本学術振興会：科学研究費助成事業 基盤研究(C)
    研究期間 : 2019年04月 -2022年03月 
    代表者 : 森山 隆太郎
     
    近年、肥満や低栄養など栄養状態の異常を起因とする不妊が家畜からヒトまで多くの動物で問題となっている。我々は長鎖脂肪酸に着目し、マウス精子の運動性に与える影響を検討した。その結果、不飽和脂肪酸は代謝エネルギーや膜の構成成分としてではなく、核内受容体であるPPARγを介して精子を活性化し、鞭毛運動を上昇させることを明らかとした。さらに、その運動上昇には、重炭酸イオン、CatSperチャネルを介した精子内へのカルシウムイオンの流入等の関与が明らかとなった。
  • 日本学術振興会：科学研究費助成事業 基盤研究(C)
    研究期間 : 2014年04月 -2017年03月 
    代表者 : 森山 隆太郎
     
    本研究では、長鎖脂肪酸がマウス精子に発現するGPR120を介してphophatidylinositol-3 kinase (PI3K)/Akt-protein kinase (Akt) およびp38 MAPK経路を活性化させることで、直進運動するマウス精子の移動速度が暴露前に比べて有意に速くなることなどを見出した。この結果は、細胞外液中の長鎖脂肪酸がシグナル分子として精子の運動性を制御するメカニズムの存在を示唆するものである。
  • 日本学術振興会：科学研究費助成事業 若手研究(B)
    研究期間 : 2011年 -2013年 
    代表者 : 森山 隆太郎
     
    本研究では、グルコース利用性の低下がAMP活性化プロテインキナーゼ (AMPK) 経路の活性化を介して黄体形成ホルモンβサブユニット (LHβ) と卵胞刺激ホルモンβサブユニット (FSHβ) 遺伝子の転写調節領域に作用し、LHとFSHの発現を抑制するメカニズムが下垂体の性腺刺激ホルモン産生細胞 (ゴナドトロフ) に存在する可能性をゴナドトロフ株化細胞であるLβT2を用いた実験により明らかとした。この結果は、家畜からヒトに至るまで多くのほ乳類で問題となっている栄養疾患による生殖障害に下垂体のゴナドトロフが関与している可能性を示唆する。
  • 日本学術振興会：科学研究費助成事業 基盤研究(C)
    研究期間 : 2009年 -2011年 
    代表者 : 福嶋 伸之; 辻内 俊文; 森山 隆太郎
     
    神経突起の分岐は生後の神経ネットワーク形成に取って必須であるがその機構は未だ不明である。今回我々はリゾホスファチジン酸(LPA)が新規情報伝達経路を介して神経分岐を促進することを示した。神経系細胞にLPA_3受容体を発現させ、LPAで刺激をすると神経分岐の形成が生じた。この作用はG_qシグナル経路の阻害により抑制された。さらに単量体型G蛋白質であるRnd2/Rho7やその効果器であるrapostlinの抑制性変異体を導入してもLPA_3を介した神経分岐形成が阻害された。LPA_3アゴニストの2(S)-OMPTやLPAは初代培養海馬神経細胞の分岐形成を引き起こしたが、この作用もG_qやRnd2の経路の阻害、あるいはLPA_3のノックダウンにより抑制された。これらの知見はLPA_3、G_qおよびRnd2を包括する新規情報伝達経路が神経ネットワーク形成に重要な役割を果たしていることを示唆している。
  • 日本学術振興会：科学研究費助成事業 若手研究(B)
    研究期間 : 2008年 -2010年 
    代表者 : 森山 隆太郎
     
    本研究により長鎖脂肪酸がシグナル分子として下垂体の性腺刺激ホルモン産生細胞(ゴナドトロフ)に直接作用することで長鎖脂肪酸受容体G-protein coupled receptor 120(GPR120)を活性化すると同時に、性腺刺激ホルモン放出ホルモン受容体(GnRH-R)発現を抑制する可能性が示された。また、ゴナドトロフのGPR120発現はエストロジェンにより制御されていることが明らかとなった。

委員歴

  • 2010年   日本繁殖生物学会   若手奨励策検討委員会委員   日本繁殖生物学会
  • 2010年   下垂体研究会   評議員   下垂体研究会

その他

  • 令和3年度 "オール近大"新型コロナウイルス感染症対策支援プロジェクト【研究-28】新型コロナウィルス感染症が霊長類の雄性生殖機能に与える影響の組織学的検討
  • 令和２年度 "オール近大"新型コロナウイルス感染症対策支援プロジェクト【研究-10】新型コロウイルスの感染症が性感染症となり得るのか検討する研究

その他のリンク

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