基本情報
研究キーワード
32研究分野
7経歴
10-
2022年4月 - 現在
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2016年1月 - 現在
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2013年9月 - 2015年12月
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2013年9月 - 2015年12月
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2008年6月 - 2013年8月
学歴
1-
- 1987年
委員歴
3-
2021年9月
受賞
2-
1999年
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1993年
論文
222-
Frontiers in Neural Circuits 19 2025年4月14日Vagus nerve stimulation (VNS) has emerged as a promising therapeutic intervention across various neurological and psychiatric conditions, including epilepsy, depression, and stroke rehabilitation; however, its mechanisms of action on neural circuits remain incompletely understood. Here, we present a novel theoretical framework based on predictive coding that conceptualizes VNS effects through differential modulation of feedforward and feedback neural circuits. Based on recent evidence, we propose that VNS shifts the balance between feedforward and feedback processing through multiple neuromodulatory systems, resulting in enhanced feedforward signal transmission. This framework integrates anatomical pathways, receptor distributions, and physiological responses to explain the influence of the VNS on neural dynamics across different spatial and temporal scales. Vagus nerve stimulation may facilitate neural plasticity and adaptive behavior through acetylcholine and noradrenaline (norepinephrine), which differentially modulate feedforward and feedback signaling. This mechanistic understanding serves as a basis for interpreting the cognitive and therapeutic outcomes across different clinical conditions. Our perspective provides a unified theoretical framework for understanding circuit-specific VNS effects and suggests new directions for investigating their therapeutic mechanisms.
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2025年2月8日Abstract The brain of a living organism enables stable information processing in response to constantly changing external environments and internal states. As one of such cortical modulation, the present study focused on the effect of vagus nerve stimulation (VNS) therapy on information representation of the auditory cortex. By quantifying sound representation using machine learning, we investigated whether VNS alters cortical information representation in a layer-specific and frequency band-specific manner. A microelectrode array meticulously mapped the band-specific power and phase-locking value of sustained activities in every layer of the rat auditory cortex. Sparse logistic regression was used to decode the test frequency from these neural characteristics. The comparison of decoding accuracy before and after the application of VNS indicated that sound representation of the high-gamma band activity was impaired in the deeper layers, i.e., layers 5 and 6, while it was slightly improved in the superficial layers, i.e., layers 2, 3, and 4. Moreover, there was an improvement of sound representation in theta band activity in the deeper layers, demonstrating the layer-specific and frequency band-specific effect of VNS. Given that the cortical laminar structure and oscillatory activity in multiple frequency bands helps the auditory cortex to act as a hub for feed-forward and feed-back pathways in various information processing, the current findings support the possibility that VNS provide complex effects on brain function by altering the balance of cortical activity between layers and frequency bands.
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Science progress 108(1) 368504251322083-368504251322083 2025年Delusional misidentification, a rare syndrome in which a patient displays persistent delusional misidentification of individuals or objects, occurs in several types of dementia. However, the pathology of delusional misidentification is still unclear, and there was no data pertaining to striate-frontal projection. Here, we report a case of delusional misidentification following frontotemporal dementia in which complex striate-frontal and some specific frontal gyrus dysfunction were observed. In our presented case, delusional misidentification progressed following frontal atrophy. Believing that her actual daughter had been replaced by her niece, her symptoms of delusional misidentification and frontal atrophy progressed in the short term, and social arrangement was necessary three months after the onset. There were no abnormal neurological findings including parkinsonism and general cognitive function test scores were preserved. Validated by dopamine transporter single-photon emission computed tomography, right unilateral striatal uptake decreased significantly without parkinsonism or Parkinson's disease. In addition, of specific concern, functional magnetic resonance images showed left opercular inferior frontal gyrus and right superior frontal gyrus dysfunctions. Our case study highlights complex striate-frontal projection and specific frontal gyrus dysfunctions associated with the pathology of delusional misidentification syndrome.
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Journal of neurosurgery. Case lessons 8(4) 2024年7月22日BACKGROUND: Chronic inflammation of the thorax, as in tuberculosis-related pyothorax, can cause secondary malignant lymphomas. However, primary malignant lymphoma of the central nervous system, specifically of the dura mater, developing after intracranial infection or inflammation has rarely been reported. Herein, the authors describe a case of primary dural lymphoma that developed secondary to subdural empyema, with an initial presentation mimicking a chronic subdural hematoma. OBSERVATIONS: A 51-year-old man had undergone single burr hole drainage for subdural empyema 2 years prior. The patient subsequently underwent multiple craniotomy and drainage procedures, with successful remission of the subdural empyema. He was subsequently referred to the authors' hospital approximately a year after his initial treatment because of a recollection of subdural fluid, which was suspected to be recurrent empyema. After another single burr hole drainage, which revealed only a subdural hematoma, a histopathological diagnosis of B-cell lymphoma of the dural/subdural membrane was made. Subsequent radiation therapy was completed, with good local control and no recurrence of the subdural hematoma confirmed at 2 months posttreatment. LESSONS: Intracranial lymphoma triggered by chronic inflammation is rare but should be considered a differential diagnosis in subdural hematomas for which the background pathology is unclear. https://thejns.org/doi/10.3171/CASE24153.
MISC
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日本てんかん学会プログラム・予稿集 (35) 137-137 2001年9月27日
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臨床脳波 43(8) 479-484 2001年8月後頭葉皮質に硬膜下電極を慢性留置された24歳女性てんかん患者の,覚醒時の皮質脳波を記録する機会を得た.本例では開眼時において,後頭葉皮質誘導には他の誘導に見られない高い周波数帯域の活動を見出した.周波数解析の結果,後頭葉誘導では約30〜300Hzに及ぶ帯域の活動が,閉眼時に比べ優位に増強していた.このガンマオシレーションは,後頭葉皮質でのみ記録され,開眼時にのみ見られる事から,光刺激に関連した活動と考えられる
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東京都医師会雑誌 54(5) 589-591 2001年6月難治性局在関連癲癇15例に対して迷走神経刺激療法(VNS)を行った.全経過中全く無効であった1例を除くと治療開始前に対する発作頻度はVNSにより減少しその後は安定する傾向がみられた.又,全般発作や複雑部分発作は単純部分発住より早期に減少する傾向がみられた.両側前頭葉に癲癇性脳波異常を有し,atypical absenceやnonconvulsive status epilepticusを呈する患者にも有効であった.又,disablingな発作ほど早期に減少する傾向は難治性癲癇の患者にとって利点の一つに挙げられた.VNSでは根治的外科治療と異なり,発作を完全に消失させることは不可能であるが,根治的外科治療が不可能又は無効な例では,低侵襲な代替治療として大いに期待される
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脳循環代謝 11(1) 12-13 1999年7月propentofylline(PPF)が,虚血耐性に及ぼす影響を検討した.2分虚血により虚血耐性を誘導し,その48時間後に5分虚血を行う砂ネズミ一過性前脳虚血モデルを用いた.薬剤は,2分虚血24時間後にvehicle,PPF10mg/kg,PPF20mg/kgを腹腔内投与し,更にnon-selective adenosine receptor antagonistであるtheophyllineを同時投与した.又,PPF20mg/kgを5分単独虚血24時間前に投与して,その影響を検討した.vehicle群では,preconditioning ischemiaによる海馬CA1錘体細胞死への保護効果が認められ,PPF10mg/kgでも同様であった.しかし,PPF20mg/kg投与群ではこれら2群に対し有意にCA1錐体細胞障害が軽く,虚血耐性増強効果が確認された.更に,この増強効果はtheophyllineの同時投与によって消失した
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日本応用磁気学会学術講演概要集 = Digest of ... annual conference on magnetics in Japan 22 369-369 1998年9月1日
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Neuropathology : official journal the Japanese Society of Neuropathology 17(Suppl.) 279-279 1997年5月26日
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Neuropathology : official journal the Japanese Society of Neuropathology 17(Suppl.) 295-295 1997年5月26日
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JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM 15(2) 205-215 1995年3月Levels of mRNAs encoding the microtubule-associated proteins MAP2b and MAP2c as well as the 70-kDa stress protein [72-kDa heat shock protein (hsp72)] were evaluated in postischemic rat brain by in situ hybridization with oligonucleotide probes corresponding to the known rat sequences. Rats were subjected to 10-min cardiac arrest, produced by compression of major thoracic vessels, followed by resuscitation. The normally expressed MAP2b mRNA showed transient twofold elevations in all hippocampal neuron populations at 6-h recirculation, followed by a return to control levels by 24 h. MAP2b hybridization was progressively lost thereafter from the vulnerable CA1 and outer cortical layers, preceding both the fall in immunoreactive MAP2b and the eventual cell loss in these regions, The depletion of MAP2b mRNA coincided with an increase in the alternatively spliced MAP2c in vulnerable regions during 12-48 h of recirculation, precisely overlapping the late component of hsp72 expression that persisted in these cell populations. Previous studies have suggested that the initial induction of hsp72 provides an index of potential postischemic injury in neuron populations that may or may not be injured, while lasting hsp72 mRNA expression is associated with cell damage. In contrast, the present results demonstrate that MAP2c expression under these conditions occurs uniquely in neuron populations subject to injury. Available evidence suggests that MAP2c expression represents a plastic response in subpopulations of neurons that will survive in these regions, although it remains to be explicitly determined whether it may also be transiently expressed in dying cells. In any case, these observations demonstrate that reexpression of developmentally regulated MAP2c mRNA is a relatively late postischemic response in vulnerable cell populations, indicating that pathways regulating MAP2 splicing may be closely associated with mechanisms of neuron injury and/or recovery.
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BRAIN EDEMA VIII 51(186) 186-188 1990年
書籍等出版物
5所属学協会
5共同研究・競争的資金等の研究課題
26-
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