ISHIGURO Masanori

写真a

Affiliation

School of Medicine, Department of Neuroscience

Job title

Assistant Professor

Profile

sapporo med university

Research Areas 【 display / non-display

  • Life sciences   Neurosurgery  

 

Research Interests 【 display / non-display

  • vascular smooth muscle

  • cerebral artery

  • 生理学

  • seronin

  • 遺伝子

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Papers 【 display / non-display

  • The Role of Aquaporin 1 in Water Retention Mechanism of Arachnoid Cysts: Insights from 3 Case Reports.

    Yasutaka Kurokawa, Masanori Ishiguro, Takayuki Kurokawa

    The American journal of case reports   24   e939834  2023.07  [International journal]

     View Summary

    BACKGROUND Although arachnoid cysts are common lesions, the pathogenesis of their continuous growth remains unclear. We aimed to identify the role of aquaporins in arachnoid cyst specimens. CASE REPORT We selected 3 cases from our own facility and examined arachnoid cyst wall specimens, which were sampled intraoperatively. Patients presented with variable symptoms, a 52-year-old man with a "heavy sensation" in the head and dysesthesia on the left hand, a 68-year-old man with unsteady gait, and finally a 26-year-old woman with a history of intermittent headaches for 10 years. Intraoperative specimens were obtained and examined. Evaluation techniques were light microscopy, immunohistochemical staining for aquaporin, and electron microscopy. Light microscopy showed that cells were arranged in epithelium-like structures forming several thick lamellae, with visible connective tissue among them. Under electron microscopic examination, cells with many or few cell organelles and with spindle-like nuclei were arranged in lamellar or flattened structures. Many vacuolizations were seen in between. Interdigitation of cells and many desmosomes were observed. All 3 cases were positive for aquaporin 1. CONCLUSIONS Our study showed that water transportation through aquaporin 1 has a potential role in the formation and expansion of arachnoid cysts.

    DOI PubMed

  • Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)

    Eichi Narimatsu, Ryuichiro Kakizaki, Kazuhito Nomura, Keigo Sawamoto, Kazunobu Takahashi, Shuji Uemura, Masanori Ishiguro

    BRAIN RESEARCH ( ELSEVIER )  1789  2022.08

     View Summary

    We investigated the effects of dexmedetomidine, a selective alpha 2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p < 0.05 was accepted as significant. Glutamate (10 mM for 10 min) completely depressed PSs and fEPSPs, which were partially recovered by the following washout for 40 min (57.4 & PLUSMN; 10.2% and 59.9 & PLUSMN; 9.8% of the control, respectively, p < 0.01, n = 6). The recoveries in PSs and fEPSPs were improved by pre-treatment and simultaneous treatment with dexmedetomidine (p < 0.01, n = 6) but were not altered by post-treatment. Dexmedetomidine alone did not alter PSs and fEPSPs. Simultaneous treatment with isoproterenol or dobutamine exacerbated the recoveries in PSs and fEPSPs (p < 0.01, n = 6), but simultaneous treatment with salbutamol, propranolol, phenylephrine or phentramine did not influence the recoveries. Simultaneous treatment with AP5 improved the recoveries in PSs and fEPSPs that were depressed by glutamate alone and by glutamate with dexmedetomidine, isoproterenol or dobutamine (p < 0.01, n = 6). Excessive glutamate depresses glutamatergic excitatory synaptic transmissions by mainly mediating NMDA receptors, and the depressed transmissions are improved by alpha 2-adrenoceptor stimulation but are exacerbated by beta 1-adrenoceptor stimulation. Dexmedetomidine has a protective effect on neuronal dysfunctions induced by excessive glutamate, which is one of the main mechanisms of the secondary damage in the central nervous system.

    DOI

  • 電流源推定に使用するMEGセンサーの選択範囲による影響に関する検討

    齊藤 秀和, 菅原 和広, 臼井 桂子, 篠崎 淳, 石黒 雅敬, 白石 秀明, 松橋 眞生, 長峯 隆

    日本生体磁気学会誌 ( 日本生体磁気学会 )  35 ( 1 ) 94 - 95  2022

  • 生体磁気計測関係のアーチファクト MEG計測において歯科矯正器具によるArtifactを認めた一例

    齊藤 秀和, 菅原 和広, 臼井 桂子, 篠崎 淳, 石黒 雅敬, 白石 秀明, 松橋 眞生, 長峯 隆

    日本生体磁気学会誌 ( 日本生体磁気学会 )  35 ( 1 ) 48 - 49  2022

  • Effects of propofol on IPSCs in CA1 and dentate gyrus cells of rat hippocampus: Propofol effects on hippocampal cells' IPSCs.

    Ishiguro M, Kobayashi S, Matsuyama K, Nagamine T

    Neuroscience research ( ELSEVIER IRELAND LTD )  143   13 - 19  2018.05  [Refereed]

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    Propofol (2, 6-diisopropylphenol) is one of the most popular intravenous anesthetic agents. In this study, we compared the effects of propofol on inhibitory postsynaptic currents (IPSCs) induced by single and paired electrical stimulations in CA1 pyramidal cells (CA1-PCs) and dentate gyrus granule cells (DG-GCs) in rat hippocampal slices using the whole cell patch-clamp technique. In the absence of propofol, the amplitude of evoked IPSC by single stimulation and decay time constants were stable in both CA1-PCs and DG-GCs for 30 min. Propofol (1 mu M and 10 mu M) increased both IPSC amplitude in CA1-PCs, but not in DG-GCs. Further, using a paired pulse stimulation protocol, the ratio of IPSC amplitudes (the second response: A2/the first response: A1) was increased by propofol in CA1, but not in DG-GCs. These results suggest that propofol selectively affects IPSCs in CA1-PCs, which is similar to previously reported actions of benzodiazepines. (C) 2018 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.

    DOI PubMed

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Misc 【 display / non-display

  • Feature of dementia disease medical center by the neurosurgeon

    Takaya Satoru, Motizuki Chie, Hatano Kimiko, Ogasawara Eriko, Oorui Motohumi, Ishiguro Masanori

    Neurosurgery for Cognitive Disorder ( Japan Society of Neurosurgery for Dementia )  3 ( 1 ) 31 - 36  2023.02

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    Our hospital was certified as the Hokkaido dementia disease medical center in 2014, and a neurosurgeon is in charge. In this study, we examined the difference in consultation status between our center by neurosurgeons and the center by psychiatrists. Differential diagnosis of dementia was performed on 248 patients who first visited our hospital from April, 2020 to March, 2021. The diagnostic categories were as follows: normal 5%, mild cognitive impairment (MCI) 37%, Alzheimer type dementia (ATD) 26%, mixed dementia 10%, dementia with Lewy bodies (DLB) 8%, vascular dementia (VaD) 6%, frontotemporal dementia1%, and others 13%. In conclusion, MCI was more common than ATD at the neurosurgeon's center, and patients were seen at an early stage of memory disturbance. In addition, there was a tendency for mixed types of VaD and ATD to be common.

    DOI

  • 反応課題遂行を中断する際の運動関連領野の関与

    矢澤 省吾, 村原 貴史, 石黒 雅敬, 長峯 隆, 竹田 里江, 豊島 貴信, 白石 秀明, 松橋 眞生

    日本生理学雑誌 ( (一社)日本生理学会 )  72 ( 12 ) 256 - 256  2010.12

  • 反応課題遂行を中断する際の運動関連領野の関与 電気刺激課題による検討

    村原 貴史, 矢澤 省吾, 豊島 貴信, 竹田 里江, 石黒 雅敬, 白石 秀明, 長峯 隆

    臨床神経生理学 ( (一社)日本臨床神経生理学会 )  38 ( 5 ) 353 - 353  2010.10

  • Recovery of hindlimb hopping locomotor function after the spinal cord hemisection in rabbits

    Kiyoji Matsuyama, Takeshi Sasaki, Takao Ishii, Masanori Ishiguro, Takashi Nagamine

    JOURNAL OF PHYSIOLOGICAL SCIENCES ( SPRINGER TOKYO )  60   S153 - S153  2010

    Research paper, summary (international conference)  

  • 運動閾値下の体性感覚弱刺激による背景脳磁場の変化

    村原 貴史, 矢澤 省吾, 豊島 貴信, 竹田 里江, 石黒 雅敬, 白石 秀明, 長峯 隆

    臨床神経生理学 ( (一社)日本臨床神経生理学会 )  37 ( 5 ) 382 - 382  2009.10

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Research Projects 【 display / non-display

  • Influences of adenosine neuromodulation on hypothermic dysfunction and protection of brain

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2022.04
    -
    2027.03
     

    成松 英智, 沢本 圭悟, 石黒 雅敬, 高橋 和伸

  • オキシヘモグロビンは神経活動を修飾する;脳スライスのシナプス活動と血管径の対比

    基盤研究(C)

    Project Year :

    2018.04
    -
    2023.03
     

    石黒 雅敬, 長峯 隆, 成松 英智

     View Summary

    コロナ感染症の蔓延と家族の死による精神的ダメージを含めた個人的環境の不備より、研究を一時中断していた。

  • 硫化水素の中枢神経系中毒機序と脳保護作用の解明

    基盤研究(C)

    Project Year :

    2016.04
    -
    2023.03
     

    成松 英智, 沢本 圭悟, 石黒 雅敬, 高橋 和伸, 高田 幸昌

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    令和3年度<海馬CA1-錐体細胞における虚血脳損傷モデルに対する低濃度硫化物イオンの影響> 令和3年度も令和2年度に引き続き,海馬スライスCA1-錐体細胞虚血脳損傷モデルに対する硫化物イオン(S2-)の影響の検証を行った.細胞外電位同時多点記録法(MEA system)を用いて,樹状突起上のEPSPを反映するfield EPSP(以下,fEPSP)および神経細胞体上の活動電位を反映するpopulation spike(以下,PS)を同時記録し,シナプス伝達変化の指標として解析した.生体の硫化水素吸入による血漿中S2-を再現する目的で,人工髄液に硫化ナトリウム(以下,Na2S)を溶解させ灌流した.PSおよびfEPSPは低酸素無グルコース人工髄液(虚血モデル)の10分間灌流(1次性脳損傷モデル介入)により完全消失したが,その後の酸素化正常人工髄液によるwashoutで部分的に回復した(過年度データ).この部分回復は,Na2S(100 mcM,10分間)の介入前および介入後投与により改善したが,同時介入では有意に変化しなかった.この成績は,すでに得られているグルタミン酸脳損傷におけるNa2S(100 mcM,10分間)の介入時の成績と類似した方向性のものであった.またNa2S(100 mcM,10分間)は単独ではPSおよびfEPSPに影響しなかった(初年度データ).以上の成績は単独では無影響な低濃度のNa2Sは,ラット海馬スライス中枢神経系シナプス伝達において虚血モデル(低酸素+無グルコース)によるシナプス伝達障害(1次性脳損傷モデル)を投与時期依存性(前および後投与時に限定的)に改善させることを示す.

  • Neural mechanisms of functional recovery of hindlimb locomotion after the spinal cord injury in quadrupeds

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2007
    -
    2008
     

    MATSUYAMA Kiyoji, ISHIGURO Masanori, SASAKI Takeshi

     View Summary

    本研究では中枢部分損傷後の歩行機能回復の神経機序解明を目的とし、下部胸髄半切断を施した除脳ウサギ歩行標本を用いて解析を進めた。この結果、脊髄半切断急性期には脊髄健常側後肢のみに歩行運動が誘発されたが、半切約1週間後には両側後肢に誘発されることを見出した。脳幹-脊髄歩行神経機構における歩行駆動信号の伝達経路の同定や末梢感覚フィードバックの機能的役割に関する解析から、脊髄半切断後の歩行機能回復は、時間経過に伴って脳幹下行性系と脊髄神経機構に生じる可塑性変化による可能性が示唆された。

  • くも膜下出血後の脳血管攣縮でのR型カルシウムチャネルを標的とする新治療法の展開

    萌芽研究

    Project Year :

    2006
    -
    2007
     

    石黒 雅敬, 寶金 清博, 石黒 雅敬

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    セロトニンは平滑筋を直接的に収縮および内皮を介して拡張させる。血管収縮には5-HT_<2A>と、5-HT_<1B>、5-HT_<1D>受容体が関係しているが、血管部位や動物の種により大きな差異がある。脳においてセロトニンは神経から拡散し、血管平滑筋には血液脳関門を介さずに到達し、脳血管や冠血管の血管攣縮あるいはその持続に影響すると考えられている。多くのセロトニン受容体サブタイプとそれぞれの作動薬および拮抗薬が見出されているが、脳血管系におけるセロトニンの意義には未解決な点が多い。今回セロトニン非存在下とセロトニン存在下の両者での塩酸サルポグレラートの血管反応を調べることを目的とした。 Wister rat(n=8)とNew Zealand white rabbit(n=11)の上小脳動脈および後大脳動脈から直径100-200μm、長さ3mmの血管を剥離し、Vessel Chamber(CH/2/A)に設定し、顕微鏡下で、Pressure Servo Control and Pump: Model PS/200/Q, FC(Living System Instrument, Burlington, VT, USA)を用いて、60mmHgの血管内圧をかけて、myogenic tone(rat12.9%±1.6,rabbit13.4%±3.1)を得た血管の血管径を測定した。 セロトニン受容体拮抗薬(5-HT2A blocker)である塩酸サルポグレラート(10^<-9>-10^<-3>M)に対する両者の反応に差を認めた。