Updated on 2024/02/21

写真a

 
KATO Daisuke
 
Organization
Graduate School of Medicine Program in Integrated Medicine Anatomy and Cell Biology Lecturer
Graduate School
Graduate School of Medicine
Undergraduate School
School of Medicine Department of Medicine
Title
Lecturer

Degree 1

  1. Doctor of Medicine ( 2013.3   Nagoya City University ) 

Research Interests 6

  1. 2光子顕微鏡

  2. オリゴデンドロサイト

  3. グリア細胞

  4. ミクログリア

  5. 神経・グリア連関

  6. 神経変性疾患

Research Areas 2

  1. Life Science / Neurology

  2. Life Science / Neuroscience-general

Research History 5

  1. 名古屋大学大学院医学系研究科 分子細胞学   講師

    2021.9

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    Country:Japan

  2. 名古屋大学大学院医学系研究科 分子細胞学   助教

    2019.10 - 2021.8

  3. 神戸大学大学院医学研究科 システム生理学   特命助教

    2019.7 - 2019.9

  4. マウントサイナイ医科大学   博士研究員

    2017.7 - 2019.9

  5. Nagoya City University   Assistant Professor

    2014.8 - 2017.3

 

Papers 53

  1. Astrocytic NKCC1 inhibits seizures by buffering Cl<SUP>-</SUP> and antagonizing neuronal NKCC1 at GABAergic synapses

    Nguyen, TD; Ishibashi, M; Sinha, AS; Watanabe, M; Kato, D; Horiuchi, H; Wake, H; Fukuda, A

    EPILEPSIA   Vol. 64 ( 12 ) page: 3389 - 3403   2023.12

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    Language:English   Publisher:Epilepsia  

    Objective: A pathological excitatory action of the major inhibitory neurotransmitter γ-aminobutyric acid (GABA) has been observed in epilepsy. Blocking the Cl− importer NKCC1 with bumetanide is expected to reduce the neuronal intracellular Cl− concentration ([Cl−]i) and thereby attenuate the excitatory GABA response. Accordingly, several clinical trials of bumetanide for epilepsy were conducted. Although NKCC1 is expressed in both neurons and glial cells, an involvement of glial NKCC1 in seizures has not yet been reported. Astrocytes maintain high [Cl−]i with NKCC1, and this gradient promotes Cl− efflux via the astrocytic GABAA receptor (GABAAR). This Cl− efflux buffers the synaptic cleft Cl− concentration to maintain the postsynaptic Cl− gradient during intense firing of GABAergic neurons, thereby sustaining its inhibitory action during seizure. In this study, we investigated the function of astrocytic NKCC1 in modulating the postsynaptic action of GABA in acute seizure models. Methods: We used the astrocyte-specific conditional NKCC1 knockout (AstroNKCC1KO) mice. The seizurelike events (SLEs) in CA1 pyramidal neurons were triggered by tetanic stimulation of stratum radiatum in acute hippocampus slices. The SLE underlying GABAAR-mediated depolarization was evaluated by applying the GABAAR antagonist bicuculline. The pilocarpine-induced seizure in vivo was monitored in adult mice by the Racine scale. The SLE duration and tetanus stimulation intensity threshold and seizure behavior in AstroNKCC1KO mice and wild-type (WT) mice were compared. Results: The AstroNKCC1KO mice were prone to seizures with lower threshold and longer duration of SLEs and larger GABAAR-mediated depolarization underlying the SLEs, accompanied by higher Racine-scored seizures. Bumetanide reduced these indicators of seizure in AstroNKCC1KO mice (which still express neuronal NKCC1), but not in the WT, both in vitro and in vivo. Significance: Astrocytic NKCC1 inhibits GABA-mediated excitatory action during seizures, whereas neuronal NKCC1 has the converse effect, suggesting opposing actions of bumetanide on these cells.

    DOI: 10.1111/epi.17784

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  2. Microglial process dynamics depend on astrocyte and synaptic activity

    Ikegami, A; Kato, D; Wake, H

    NAGOYA JOURNAL OF MEDICAL SCIENCE   Vol. 85 ( 4 ) page: 772 - 778   2023.11

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    Language:English   Publisher:Nagoya Journal of Medical Science  

    Microglial processes survey the brain parenchyma, but it is unknown whether this process is influenced by the cell activity of nearby microglia under physiological conditions. Herein, we showed that microglial process dynamics differ when facilitated by astrocytic activity and pre-synaptic activity. The results revealed distinct microglial process dynamics associated with the activity of other brain cells.

    DOI: 10.18999/nagjms.85.4.772

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  3. Fatal remote cerebral hemorrhage at a site of a microbleed immediately after intravenous thrombolysis

    Oomura M., Fujioka T., Uchida Y., Kato D., Nishikawa Y., Matsukawa N.

    Neurology and Clinical Neuroscience   Vol. 5 ( 4 ) page: 118 - 120   2017.7

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    Publisher:Neurology and Clinical Neuroscience  

    We report a patient with ischemic stroke who was treated with intravenous alteplase and subsequently developed a fatal pontine hemorrhage during cerebral angiography. An 88-year-old woman presented with right hemiplegia and aphasia. Magnetic resonance angiography at onset showed occlusion of the left middle cerebral artery. T2*-weighted magnetic resonance imaging showed a cerebral microbleed in the pons. She was treated with intravenous alteplase followed by cerebral angiography. Left carotid angiography showed recanalization of the left middle cerebral artery, and neurointervention was not carried out. During the angiography, she became comatose. Computed tomography showed a massive pontine hemorrhage. The hemorrhage was considered to be attributable to the microbleed. The variety of time phases of cerebral microbleeds have been elucidated; there are a subset of lesions reflecting acute or subacute microhemorrhages. It is considered that expansion of a pontine microbleed induced by alteplase caused a fatal remote cerebral hemorrhage in the present case.

    DOI: 10.1111/ncn3.12124

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  4. Activity-dependent oligodendrocyte calcium dynamics and their changes in Alzheimer's disease. International journal

    Kenji Yoshida, Daisuke Kato, Shouta Sugio, Ikuko Takeda, Hiroaki Wake

    Frontiers in cellular neuroscience   Vol. 17   page: 1154196 - 1154196   2023.10

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    Oligodendrocytes (OCs) form myelin around axons, which is dependent on neuronal activity. This activity-dependent myelination plays a crucial role in training and learning. Previous studies have suggested that neuronal activity regulates proliferation and differentiation of oligodendrocyte precursor cells (OPCs) and myelination. In addition, deficient activity-dependent myelination results in impaired motor learning. However, the functional response of OC responsible for neuronal activity and their pathological changes is not fully elucidated. In this research, we aimed to understand the activity-dependent OC responses and their different properties by observing OCs using in vivo two-photon microscopy. We clarified that the Ca2+ activity in OCs is neuronal activity dependent and differentially regulated by neurotransmitters such as glutamate or adenosine triphosphate (ATP). Furthermore, in 5-month-old mice models of Alzheimer's disease, a period before the appearance of behavioral abnormalities, the elevated Ca2+ responses in OCs are ATP dependent, suggesting that OCs receive ATP from damaged tissue. We anticipate that our research will help in determining the correct therapeutic strategy for neurodegenerative diseases beyond the synapse.

    DOI: 10.3389/fncel.2023.1154196

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  5. Microglia enable cross-modal plasticity by removing inhibitory synapses. International journal

    Akari Hashimoto, Nanami Kawamura, Etsuko Tarusawa, Ikuko Takeda, Yuki Aoyama, Nobuhiko Ohno, Mio Inoue, Mai Kagamiuchi, Daisuke Kato, Mami Matsumoto, Yoshihiro Hasegawa, Junichi Nabekura, Anne Schaefer, Andrew J Moorhouse, Takeshi Yagi, Hiroaki Wake

    Cell reports   Vol. 42 ( 5 ) page: 112383 - 112383   2023.5

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    Cross-modal plasticity is the repurposing of brain regions associated with deprived sensory inputs to improve the capacity of other sensory modalities. The functional mechanisms of cross-modal plasticity can indicate how the brain recovers from various forms of injury and how different sensory modalities are integrated. Here, we demonstrate that rewiring of the microglia-mediated local circuit synapse is crucial for cross-modal plasticity induced by visual deprivation (monocular deprivation [MD]). MD relieves the usual inhibition of functional connectivity between the somatosensory cortex and secondary lateral visual cortex (V2L). This results in enhanced excitatory responses in V2L neurons during whisker stimulation and a greater capacity for vibrissae sensory discrimination. The enhanced cross-modal response is mediated by selective removal of inhibitory synapse terminals on pyramidal neurons by the microglia in the V2L via matrix metalloproteinase 9 signaling. Our results provide insights into how cortical circuits integrate different inputs to functionally compensate for neuronal damage.

    DOI: 10.1016/j.celrep.2023.112383

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  6. Direct Enhancement Effect of Hippocampal Cholinergic Neurostimulating Peptide on Cholinergic Activity in the Hippocampus. International journal

    Yuta Madokoro, Daisuke Kato, Yo Tsuda, Itsumi Arakawa, Kengo Suzuki, Toyohiro Sato, Masayuki Mizuno, Yuto Uchida, Kosei Ojika, Noriyuki Matsukawa

    International journal of molecular sciences   Vol. 24 ( 10 )   2023.5

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    The cholinergic efferent network from the medial septal nucleus to the hippocampus is crucial for learning and memory. This study aimed to clarify whether hippocampal cholinergic neurostimulating peptide (HCNP) has a rescue function in the cholinergic dysfunction of HCNP precursor protein (HCNP-pp) conditional knockout (cKO). Chemically synthesized HCNP or a vehicle were continuously administered into the cerebral ventricle of HCNP-pp cKO mice and littermate floxed (control) mice for two weeks via osmotic pumps. We immunohistochemically measured the cholinergic axon volume in the stratum oriens and functionally evaluated the local field potential in the CA1. Furthermore, choline acetyltransferase (ChAT) and nerve growth factor (NGF) receptor (TrkA and p75NTR) abundances were quantified in wild-type (WT) mice administered HCNP or the vehicle. As a result, HCNP administration morphologically increased the cholinergic axonal volume and electrophysiological theta power in HCNP-pp cKO and control mice. Following the administration of HCNP to WT mice, TrkA and p75NTR levels also decreased significantly. These data suggest that extrinsic HCNP may compensate for the reduced cholinergic axonal volume and theta power in HCNP-pp cKO mice. HCNP may function complementarily to NGF in the cholinergic network in vivo. HCNP may represent a therapeutic candidate for neurological diseases with cholinergic dysfunction, e.g., Alzheimer's disease and Lewy body dementia.

    DOI: 10.3390/ijms24108916

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  7. CD206+ macrophages transventricularly infiltrate the early embryonic cerebral wall to differentiate into microglia Reviewed

    Yuki Hattori, Daisuke Kato, Futoshi Murayama, Sota Koike, Hisa Asai, Ayato Yamasaki, Yu Naito, Ayano Kawaguchi, Hiroyuki Konishi, Marco Prinz, Takahiro Masuda, Hiroaki Wake, Takaki Miyata

    Cell Reports   Vol. 42 ( 2 ) page: 112092 - 112092   2023.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.celrep.2023.112092

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  8. Myelinated axon as a plastic cable regulating brain functions. International journal

    Shouta Sugio, Daisuke Kato, Hiroaki Wake

    Neuroscience research   Vol. 187   page: 45 - 51   2023.2

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    Each oligodendrocyte (OC) forms myelin approximately in around 10 different axons to coordinate information transfer by regulating conduction velocity in the central nervous system (CNS). In the classical view, myelin has been considered a static structure that rarely turns over under healthy conditions because myelin tightly holds axons by their laminar complex structure. However, in recent decades, the classical views of static myelin have been renewed with pioneering studies that showed plastic changes in myelin throughout life with new experiences, such as the acquisition of new motor skills and the formation of memory. These changes in myelin regulate conduction velocity to optimize the temporal pattern of neuronal circuit activity among distinct brain regions associated with skill learning and memory. Here, we introduce pioneering studies and discuss the implications of plastic myelin on neural circuits and brain function.

    DOI: 10.1016/j.neures.2022.11.002

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  9. [Microglial regulation of brain function and pathological changes].

    Hiroaki Wake, Akari Hashimoto, Daisuke Kato, Ikuko Takeda

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica   Vol. 158 ( 5 ) page: 359 - 361   2023

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:The Japanese Pharmacological Society  

    Microglia are the only immune cells in the central nervous system. It has been shown that microglia actively regulate the number of neurons by participating in the cell death of neural stem cells during development and maturation. In addition, recent optical techniques have enabled in vivo imaging, which has revealed the function of microglia on synapses. Microglia regularly monitor synaptic activity and remove synapses that show abnormal activity in the event of brain infarction or other disorders. During development, microglia contribute to the formation of immature synapses by contacting dendrites during early synapse formation, and they are also involved in the de-synaptic process by selectively removing weakly active synapses through the use of classical complement cascade signaling. Furthermore, these abnormalities are known to contribute to the development of autism during development and to the development of Alzheimer's disease during maturation. In addition to this, microglia also contribute to plastic changes in synapses during the learning process in maturation. Furthermore, by modifying synaptic activity, microglia are known to be involved in changes in the activity of neuronal circuits. In addition to these synaptic functions, microglia are also known to be involved in the permeability of the blood-brain barrier. In this chapter, these functions will be summarized and discussed.

    DOI: 10.1254/fpj.23010

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  10. Evaluation and Manipulation of Neural Activity using Two-Photon Holographic Microscopy. International journal

    Daisuke Kato, Xiangyu Quan, Yuta Tanisumi, Zhongtian Guo, Mitsuhiro Morita, Tetsuya Takiguchi, Osamu Matoba, Hiroaki Wake

    Journal of visualized experiments : JoVE   Vol. 2022 ( 187 )   2022.9

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    Recent advances in optical bioimaging and optogenetics have enabled the visualization and manipulation of biological phenomena, including cellular activities, in living animals. In the field of neuroscience, detailed neural activity related to brain functions, such as learning and memory, has now been revealed, and it has become feasible to artificially manipulate this activity to express brain functions. However, the conventional evaluation of neural activity by two-photon Ca2+ imaging has the problem of low temporal resolution. In addition, manipulation of neural activity by conventional optogenetics through the optic fiber can only simultaneously regulate the activity of neurons with the same genetic background, making it difficult to control the activity of individual neurons. To solve this issue, we recently developed a microscope with a high spatiotemporal resolution for biological applications by combining optogenetics with digital holographic technology that can modify femtosecond infrared laser beams. Here, we describe protocols for the visualization, evaluation, and manipulation of neural activity, including the preparation of samples and operation of a two-photon holographic microscope (Figure 1). These protocols provide accurate spatiotemporal information on neural activity, which may be useful for elucidating the pathogenesis of neuropsychiatric disorders that lead to abnormalities in neural activity.

    DOI: 10.3791/64205

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  11. A Piezo1/KLF15/IL-6 axis mediates immobilization-induced muscle atrophy International journal

    Yu Hirata, Kazuhiro Nomura, Daisuke Kato, Yoshihisa Tachibana, Takahiro Niikura, Kana Uchiyama, Tetsuya Hosooka, Tomoaki Fukui, Keisuke Oe, Ryosuke Kuroda, Yuji Hara, Takahiro Adachi, Koji Shibasaki, Hiroaki Wake, Wataru Ogawa

    Journal of Clinical Investigation   Vol. 132 ( 10 ) page: 1 - 13   2022.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:American Society for Clinical Investigation  

    Although immobility is a common cause of muscle atrophy, the mechanism underlying this causality is unclear. We here show that Krüppel-like factor 15 (KLF15) and IL-6 are upregulated in skeletal muscle of limb-immobilized mice and that mice with KLF15 deficiency in skeletal muscle or with systemic IL-6 deficiency are protected from immobility-induced muscle atrophy. A newly developed Ca2+ bioimaging revealed that the cytosolic Ca2+ concentration ([Ca2+]i) of skeletal muscle is reduced to below the basal level by immobilization, which is associated with the downregulation of Piezo1. Acute disruption of Piezo1 in skeletal muscle induced Klf15 and Il6 expression as well as muscle atrophy, which was prevented by antibodies against IL-6. A role for the Piezo1/KLF15/IL-6 axis in immobility-induced muscle atrophy was validated in human samples. Our results thus uncover a paradigm for Ca2+ signaling in that a decrease in [Ca2+]i from the basal level triggers a defined biological event.

    DOI: 10.1172/JCI154611

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  12. Elucidation of the neurological effects of clothianidin exposure at the no-observed-adverse-effect level (NOAEL) using two-photon microscopy &lt;i&gt;in vivo&lt;/i&gt; imaging

    Misaki NISHI, Shouta SUGIO, Tetsushi HIRANO, Daisuke KATO, Hiroaki WAKE, Asuka SHODA, Midori MURATA, Yoshinori IKENAKA, Yoshiaki TABUCHI, Youhei MANTANI, Toshifumi YOKOYAMA, Nobuhiko HOSHI

    Journal of Veterinary Medical Science   Vol. 84 ( 4 ) page: 585 - 592   2022.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Japanese Society of Veterinary Science  

    Neonicotinoid pesticides (NNs) cause behavioral abnormalities in mammals, raising concerns about their effects on neural circuit activity. We herein examined the neurological effects of the NN clothianidin (CLO) by in vivo Ca2+ imaging using two-photon microscopy. Mice were fed the no-observed-adverse-effect-level (NOAEL) dose of CLO for 2 weeks and their neuronal activity in the primary somatosensory cortex (S1) was observed weekly for 2 weeks. CLO exposure caused a sustained influx of Ca2+ in neurons in the S1 2/3 layers, indicating hyperactivation of neurons. In addition, microarray gene expression analysis suggested the induction of neuroinflammation and changes in synaptic activity. These results demonstrate that exposure to the NOAEL dose of CLO can overactivate neurons and disrupt neuronal homeostasis.

    DOI: 10.1292/jvms.22-0013

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  13. A Piezo1/KLF15/IL-6 axis mediates immobilization-induced muscle atrophy Invited Reviewed

    Yu Hirata, Kazuhiro Nomura, Daisuke Kato, Yoshihisa Tachibana, Takahiro Niikura, Kana Uchiyama, Tetsuya Hosooka, Tomoaki Fukui, Keisuke Oe, Ryosuke Kuroda, Yuji Hara, Takahiro Adachi, Koji Shibasaki, Hiroaki Wake, Wataru Ogawa

    Journal of Clinical Investigation     2022.3

  14. Holographic microscope and its biological application Invited Reviewed

        2021.11

  15. [A New Outlook on Mental Disorders: Pathological Dynamics of Glial Cells].

    Yuko Arioka, Daisuke Kato, Hiroaki Wake, Norio Ozaki

    Brain and nerve = Shinkei kenkyu no shinpo   Vol. 73 ( 7 ) page: 787 - 794   2021.7

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    The pathophysiology of mental disorders remains unknown. This causes many gaps in pathophysiology, diagnosis, and treatment of mental disorders. To close these gaps, a new perspective, which is not bound by the existing diagnostic classifications or pathological hypotheses for mental disorders, is required. Recently, it has been reported that glial cells play active roles in normal brain function and circuit formation, and their disruption results in the onset of mental disorders. Here, we discuss mental disorders from the perspective of glial cell-related pathophysiology, along with our current efforts and research.

    DOI: 10.11477/mf.1416201836

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  16. Pain induces stable, active microcircuits in the somatosensory cortex that provide a therapeutic target.

    Okada T, Kato D, Nomura Y, Obata N, Quan X, Morinaga A, Yano H, Guo Z, Aoyama Y, Tachibana Y, Moorhouse AJ, Matoba O, Takiguchi T, Mizobuchi S, Wake H

    Science advances   Vol. 7 ( 12 )   2021.3

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  17. Possible correlated variation of GABAA receptor α3 expression with hippocampal cholinergic neurostimulating peptide precursor protein in the hippocampus. International journal

    Kenichi Adachi, Daisuke Kato, Tomoaki Kahyo, Tomokazu Konishi, Toyohiro Sato, Yuta Madokoro, Masayuki Mizuno, Hiroyasu Akatsu, Mitsutoshi Setou, Noriyuki Matsukawa

    Biochemical and biophysical research communications   Vol. 542   page: 80 - 86   2021.2

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    Cholinergic neural activation from the medial septal nucleus to hippocampus plays a crucial role in episodic memory as a regulating system for glutamatergic neural activation in the hippocampus. As a candidate regulating factor for acetylcholine synthesis in the medial septal nucleus, hippocampal cholinergic neurostimulating peptide (HCNP) was purified from the soluble fraction of young adult rat hippocampus. HCNP is released from its precursor protein (HCNP-pp), also referred to as phosphatidylethanolamine-binding protein 1. We recently reported that HCNP-pp conditional knockout (KO) mice, in which the HCNP-pp gene was knocked out at 3 months of age by tamoxifen injection, display no significant behavioral abnormalities, whereas HCNP-pp KO mice have a diminished cholinergic projection to CA1 and a decreased of theta activity in CA1. In this study, to address whether HCNP-pp reduction in early life is associated with behavioral changes, we evaluated the behavior of HCNP-pp KO mice in which HCNP-pp was downregulated from an early phase (postnatal days 14-28). As unexpected, HCNP-pp KO mice had no behavioral deficits. However, a significant positive correlation between HCNP-pp and gamma-aminobutyric acid A (GABAA) receptor α3 subunit mRNA expression was found in individuals. This finding suggests involvement of HCNP-pp in regulating GABAA receptor α3 gene expression.

    DOI: 10.1016/j.bbrc.2021.01.010

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  18. Post-error recruitment of frontal sensory cortical projections promotes attention in mice. International journal

    Kevin J Norman, Justin S Riceberg, Hiroyuki Koike, Julia Bateh, Sarah E McCraney, Keaven Caro, Daisuke Kato, Ana Liang, Kazuhiko Yamamuro, Meghan E Flanigan, Korey Kam, Elisa N Falk, Daniel M Brady, Christina Cho, Masato Sadahiro, Kohei Yoshitake, Priscilla Maccario, Michael P Demars, Leah Waltrip, Andrew W Varga, Scott J Russo, Mark G Baxter, Matthew L Shapiro, Peter H Rudebeck, Hirofumi Morishita

    Neuron     2021.2

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    The frontal cortex, especially the anterior cingulate cortex area (ACA), is essential for exerting cognitive control after errors, but the mechanisms that enable modulation of attention to improve performance after errors are poorly understood. Here we demonstrate that during a mouse visual attention task, ACA neurons projecting to the visual cortex (VIS; ACAVIS neurons) are recruited selectively by recent errors. Optogenetic manipulations of this pathway collectively support the model that rhythmic modulation of ACAVIS neurons in anticipation of visual stimuli is crucial for adjusting performance following errors. 30-Hz optogenetic stimulation of ACAVIS neurons in anesthetized mice recapitulates the increased gamma and reduced theta VIS oscillatory changes that are associated with endogenous post-error performance during behavior and subsequently increased visually evoked spiking, a hallmark feature of visual attention. This frontal sensory neural circuit links error monitoring with implementing adjustments of attention to guide behavioral adaptation, pointing to a circuit-based mechanism for promoting cognitive control.

    DOI: 10.1016/j.neuron.2021.02.001

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  19. Myelin plasticity modulates neural circuitry required for learning and behavior. International journal

    Daisuke Kato, Hiroaki Wake

    Neuroscience research     2021.1

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    Oligodendrocytes, which form the myelin sheaths that insulate axons, regulate conduction velocity. Myelinated axons make up the brain's white matter and contribute to the efficiency of information processing by regulating the timing of neural activity. Traditionally, it has been thought that myelin is a static, inactive insulator around the axon. However, recent studies in humans using magnetic resonance imaging have shown that structural changes in the white matter occur during learning and training, suggesting that 1) white matter change depends on neural activity and 2) activity-dependent changes in white matter are essential for learning and behavior. Furthermore, suppression of oligodendrocytes and their progenitor cells leads to deficits in motor learning and remote fear memory consolidation, suggesting a causal relationship between glial function and the learning process. However, for technical reasons, it remains unclear how myelin-generating glia modulate neural circuitry and what underlying mechanisms they employ to affect learning and behavior. Recent advances in optical and genetic techniques have helped elucidate this mechanism. In this review, we highlight evidence that neural activities regulated by myelin plasticity play a pivotal role in learning and behavior and provide further insight into possible therapeutic targets for treating diseases accompanied by myelin impairment.

    DOI: 10.1016/j.neures.2020.12.005

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  20. Maternal immune activation induces sustained changes in fetal microglia motility. International journal

    Kana Ozaki, Daisuke Kato, Ako Ikegami, Akari Hashimoto, Shouta Sugio, Zhongtian Guo, Midori Shibushita, Tsuyako Tatematsu, Koichiro Haruwaka, Andrew J Moorhouse, Hideto Yamada, Hiroaki Wake

    Scientific reports   Vol. 10 ( 1 ) page: 21378 - 21378   2020.12

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    Maternal infection or inflammation causes abnormalities in brain development associated with subsequent cognitive impairment and in an increased susceptibility to schizophrenia and autism spectrum disorders. Maternal immune activation (MIA) and increases in serum cytokine levels mediates this association via effects on the fetal brain, and microglia can respond to maternal immune status, but consensus on how microglia may respond is lacking and no-one has yet examined if microglial process motility is impaired. In this study we investigated how MIA induced at two different gestational ages affected microglial properties at different developmental stages. Immune activation in mid-pregnancy increased IL-6 expression in embryonic microglia, but failed to cause any marked changes in morphology either at E18 or postnatally. In contrast MIA, particularly when induced earlier (at E12), caused sustained alterations in the patterns of microglial process motility and behavioral deficits. Our research has identified an important microglial property that is altered by MIA and which may contribute to the underlying pathophysiological mechanisms linking maternal immune status to subsequent risks for cognitive disease.

    DOI: 10.1038/s41598-020-78294-2

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  21. A prefrontal-paraventricular thalamus circuit requires juvenile social experience to regulate adult sociability in mice. International journal

    Kazuhiko Yamamuro, Lucy K Bicks, Michael B Leventhal, Daisuke Kato, Susanna Im, Meghan E Flanigan, Yury Garkun, Kevin J Norman, Keaven Caro, Masato Sadahiro, Klas Kullander, Schahram Akbarian, Scott J Russo, Hirofumi Morishita

    Nature neuroscience   Vol. 23 ( 10 ) page: 1240 - 1252   2020.10

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    Juvenile social isolation reduces sociability in adulthood, but the underlying neural circuit mechanisms are poorly understood. We found that, in male mice, 2 weeks of social isolation immediately following weaning leads to a failure to activate medial prefrontal cortex neurons projecting to the posterior paraventricular thalamus (mPFC→pPVT) during social exposure in adulthood. Chemogenetic or optogenetic suppression of mPFC→pPVT activity in adulthood was sufficient to induce sociability deficits without affecting anxiety-related behaviors or preference toward rewarding food. Juvenile isolation led to both reduced excitability of mPFC→pPVT neurons and increased inhibitory input drive from low-threshold-spiking somatostatin interneurons in adulthood, suggesting a circuit mechanism underlying sociability deficits. Chemogenetic or optogenetic stimulation of mPFC→pPVT neurons in adulthood could rescue the sociability deficits caused by juvenile isolation. Our study identifies a pair of specific medial prefrontal cortex excitatory and inhibitory neuron populations required for sociability that are profoundly affected by juvenile social experience.

    DOI: 10.1038/s41593-020-0695-6

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  22. Iron leakage owing to blood-brain barrier disruption in small vessel disease CADASIL. International journal

    Yuto Uchida, Hirohito Kan, Keita Sakurai, Nobuyuki Arai, Shohei Inui, Susumu Kobayashi, Daisuke Kato, Yoshino Ueki, Noriyuki Matsukawa

    Neurology   Vol. 95 ( 9 ) page: e1188 - e1198   2020.9

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    OBJECTIVE: To assess the relationship among iron accumulation, blood-brain barrier (BBB) damage, and cognitive function in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). METHODS: We enrolled 21 patients with NOTCH3 mutations and 21 age-matched healthy controls in this cross-sectional study. All participants underwent global physical and cognitive assessments and brain MRI using voxel-based quantitative susceptibility mapping (QSM; iron deposition measure) and dynamic contrast-enhanced MRI (BBB permeability measure). We compared behavioral and imaging data between the groups and analyzed the correlations in each group. RESULTS: Among 21 NOTCH3 mutation carriers, 10 were symptomatic and 11 asymptomatic. Montreal Cognitive Assessment scores were significantly different among the groups (symptomatic < asymptomatic < control participants). Voxel-based QSM analysis revealed that the symptomatic group had higher QSM values than did the asymptomatic group in the putamen, caudate nucleus, temporal pole, and centrum semiovale. These QSM values were positively correlated with regional BBB permeabilities (putamen: r = 0.57, p = 0.006; caudate nucleus: r = 0.51, p = 0.019; temporal pole: r = 0.48, p = 0.030; centrum semiovale: r = 0.45, p = 0.044) and negatively correlated with Montreal Cognitive Assessment scores (caudate nucleus: r = -0.53, p = 0.012; temporal pole: r = -0.56, p = 0.008). CONCLUSIONS: This study showed that cerebral iron burden was associated with regional BBB permeability and cognitive dysfunction in patients with CADASIL, highlighting the potential of these imaging techniques as auxiliary biomarkers to monitor the course of small vessel disease.

    DOI: 10.1212/WNL.0000000000010148

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  23. Selection of treatment for ictal asystole patients based on EEG and ECG with temporary cardiac pacing. International journal

    Yuta Madokoro, Daisuke Kato, Kiyohito Terada, Masayuki Mizuno, Noriyuki Matsukawa

    Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology   Vol. 41 ( 7 ) page: 1973 - 1975   2020.7

  24. Prefrontal parvalbumin interneurons require juvenile social experience to establish adult social behavior. International journal

    Lucy K Bicks, Kazuhiko Yamamuro, Meghan E Flanigan, Julia Minjung Kim, Daisuke Kato, Elizabeth K Lucas, Hiroyuki Koike, Michelle S Peng, Daniel M Brady, Sandhya Chandrasekaran, Kevin J Norman, Milo R Smith, Roger L Clem, Scott J Russo, Schahram Akbarian, Hirofumi Morishita

    Nature communications   Vol. 11 ( 1 ) page: 1003 - 1003   2020.2

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    Social isolation during the juvenile critical window is detrimental to proper functioning of the prefrontal cortex (PFC) and establishment of appropriate adult social behaviors. However, the specific circuits that undergo social experience-dependent maturation to regulate social behavior are poorly understood. We identify a specific activation pattern of parvalbumin-positive interneurons (PVIs) in dorsal-medial PFC (dmPFC) prior to an active bout, or a bout initiated by the focal mouse, but not during a passive bout when mice are explored by a stimulus mouse. Optogenetic and chemogenetic manipulation reveals that brief dmPFC-PVI activation triggers an active social approach to promote sociability. Juvenile social isolation decouples dmPFC-PVI activation from subsequent active social approach by freezing the functional maturation process of dmPFC-PVIs during the juvenile-to-adult transition. Chemogenetic activation of dmPFC-PVI activity in the adult animal mitigates juvenile isolation-induced social deficits. Therefore, social experience-dependent maturation of dmPFC-PVI is linked to long-term impacts on social behavior.

    DOI: 10.1038/s41467-020-14740-z

    PubMed

  25. Motor learning requires myelination to reduce asynchrony and spontaneity in neural activity. International journal

    Daisuke Kato, Hiroaki Wake, Philip R Lee, Yoshihisa Tachibana, Riho Ono, Shouta Sugio, Yukio Tsuji, Yasuyo H Tanaka, Yasuhiro R Tanaka, Yoshito Masamizu, Riichiro Hira, Andrew J Moorhouse, Nobuaki Tamamaki, Kazuhiro Ikenaka, Noriyuki Matsukawa, R Douglas Fields, Junichi Nabekura, Masanori Matsuzaki

    Glia   Vol. 68 ( 1 ) page: 193 - 210   2020.1

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    Myelination increases the conduction velocity in long-range axons and is prerequisite for many brain functions. Impaired myelin regulation or impairment of myelin itself is frequently associated with deficits in learning and cognition in neurological and psychiatric disorders. However, it has not been revealed what perturbation of neural activity induced by myelin impairment causes learning deficits. Here, we measured neural activity in the motor cortex during motor learning in transgenic mice with a subtle impairment of their myelin. This deficit in myelin impaired motor learning, and was accompanied by a decrease in the amplitude of movement-related activity and an increase in the frequency of spontaneous activity. Thalamocortical axons showed variability in axonal conduction with a large spread in the timing of postsynaptic cortical responses. Repetitive pairing of forelimb movements with optogenetic stimulation of thalamocortical axon terminals restored motor learning. Thus, myelin regulation helps to maintain the synchrony of cortical spike-time arrivals through long-range axons, facilitating the propagation of the information required for learning. Our results revealed the pathological neuronal circuit activity with impaired myelin and suggest the possibility that pairing of noninvasive brain stimulation with relevant behaviors may ameliorate cognitive and behavioral abnormalities in diseases with impaired myelination.

    DOI: 10.1002/glia.23713

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  26. Implications for White Matter Vulnerability to Anti-interleukin-6 Receptor Antibody Treatment.

    Daisuke Kato

    Internal medicine (Tokyo, Japan)   Vol. 59 ( 22 ) page: 2809 - 2810   2020

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    DOI: 10.2169/internalmedicine.5765-20

    Web of Science

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  27. Dual microglia effects on blood brain barrier permeability induced by systemic inflammation. International journal

    Koichiro Haruwaka, Ako Ikegami, Yoshihisa Tachibana, Nobuhiko Ohno, Hiroyuki Konishi, Akari Hashimoto, Mami Matsumoto, Daisuke Kato, Riho Ono, Hiroshi Kiyama, Andrew J Moorhouse, Junichi Nabekura, Hiroaki Wake

    Nature communications   Vol. 10 ( 1 ) page: 5816 - 5816   2019.12

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    Microglia survey brain parenchyma, responding to injury and infections. Microglia also respond to systemic disease, but the role of blood-brain barrier (BBB) integrity in this process remains unclear. Using simultaneous in vivo imaging, we demonstrated that systemic inflammation induces CCR5-dependent migration of brain resident microglia to the cerebral vasculature. Vessel-associated microglia initially maintain BBB integrity via expression of the tight-junction protein Claudin-5 and make physical contact with endothelial cells. During sustained inflammation, microglia phagocytose astrocytic end-feet and impair BBB function. Our results show microglia play a dual role in maintaining BBB integrity with implications for elucidating how systemic immune-activation impacts neural functions.

    DOI: 10.1038/s41467-019-13812-z

    Web of Science

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  28. Reduced Cholinergic Activity in the Hippocampus of Hippocampal Cholinergic Neurostimulating Peptide Precursor Protein Knockout Mice. International journal

    Yuta Madokoro, Yuta Yoshino, Daisuke Kato, Toyohiro Sato, Masayuki Mizuno, Tetsuko Kanamori, Masamitsu Shimazawa, Hideki Hida, Hideaki Hara, Mari Yoshida, Cesario V Borlongan, Kosei Ojika, Noriyuki Matsukawa

    International journal of molecular sciences   Vol. 20 ( 21 )   2019.10

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    The cholinergic efferent network from the medial septal nucleus to the hippocampus has an important role in learning and memory processes. This cholinergic projection can generate theta oscillations in the hippocampus to efficiently encode novel information. Hippocampal cholinergic neurostimulating peptide (HCNP) induces acetylcholine synthesis in medial septal nuclei. HCNP is processed from the N-terminal region of a 186 amino acid, 21 kD HCNP precursor protein called HCNP-pp (also known as Raf kinase inhibitory protein (RKIP) and phosphatidylethanolamine-binding protein 1 (PEBP1)). In this study, we generated HCNP-pp knockout (KO) mice and assessed their cholinergic septo-hippocampal projection, local field potentials in CA1, and behavioral phenotypes. No significant behavioral phenotype was observed in HCNP-pp KO mice. However, theta power in the CA1 of HCNP-pp KO mice was significantly reduced because of fewer cholineacetyltransferase-positive axons in the CA1 stratum oriens. These observations indicated disruption of cholinergic activity in the septo-hippocampal network. Our study demonstrates that HCNP may be a cholinergic regulator in the septo-hippocampal network.

    DOI: 10.3390/ijms20215367

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  29. Voxel-based quantitative susceptibility mapping in Parkinson's disease with mild cognitive impairment. International journal

    Yuto Uchida, Hirohito Kan, Keita Sakurai, Nobuyuki Arai, Daisuke Kato, Shoji Kawashima, Yoshino Ueki, Noriyuki Matsukawa

    Movement disorders : official journal of the Movement Disorder Society   Vol. 34 ( 8 ) page: 1164 - 1173   2019.8

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    OBJECTIVE: Brain iron accumulation has been proposed as one of the pathomechanisms in Parkinson's disease (PD). This study aimed to examine the whole-brain pattern of iron accumulation associated with cognitive impairment in patients with PD using voxel-based quantitative susceptibility mapping analysis. METHODS: We enrolled 24 patients with PD and mild cognitive impairment, 22 patients with PD and normal cognition, and 20 age-matched healthy controls in this cross-sectional study. All participants underwent global cognitive and physical assessments and brain MRI. Using a combined method of voxel-based morphometry and quantitative susceptibility mapping, we compared the voxel-wise magnetic susceptibility of the whole brain between the groups and analyzed its correlation with the cognitive and behavioral data. RESULTS: The PD and mild cognitive impairment group had lower Montreal Cognitive Assessment (MoCA) score than the PD and normal cognition and healthy control groups. There were no gray matter volumetric differences between the groups. In contrast, the voxel-based quantitative susceptibility mapping analysis showed that the PD and mild cognitive impairment group had significantly higher quantitative susceptibility mapping values in the cuneus, precuneus, caudate head, fusiform gyrus, and orbitofrontal cortex than did the PD and normal cognition group. These quantitative susceptibility mapping values were negatively correlated with the MoCA scores in the PD patients (cuneus: r = -0.510, P < .001; caudate head: r = -0.458, P = 0.002). CONCLUSIONS: This study suggests that cognitive impairment in PD is associated with cerebral iron burden and highlights the potential of quantitative susceptibility mapping as an auxiliary biomarker for early evaluation of cognitive decline in patients with PD. © 2019 International Parkinson and Movement Disorder Society.

    DOI: 10.1002/mds.27717

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  30. Anatomical Links between White Matter Hyperintensity and Medial Temporal Atrophy Reveal Impairment of Executive Functions. International journal

    Takehiko Yamanaka, Yuto Uchida, Keita Sakurai, Daisuke Kato, Masayuki Mizuno, Toyohiro Sato, Yuta Madokoro, Yuko Kondo, Ayuko Suzuki, Yoshino Ueki, Fumiyasu Ishii, Cesar V Borlongan, Noriyuki Matsukawa

    Aging and disease   Vol. 10 ( 4 ) page: 711 - 718   2019.8

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    Although several studies have demonstrated correlation between white matter hyperintensities (WMH) and impairment of executive functions, the underlying anatomical-functional relationships are not fully understood. The present study sought to investigate the correlations between the volume of WMH and medial temporal lobe atrophy (MTA) using quantitative magnetic resonance image (MRI) and a variety of executive function assessments. A total of 91 patients ranging in age from 58 to 90 years with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or early phase AD were recruited from the outpatient clinic at the Department of Neurology of Nagoya City University Hospital. We administered neuropsychological batteries evaluating verbal memory, orientation, spatial ability, sustained attention, and a variety of executive functions, including verbal fluency, flexibility, inhibition, and working memory. Quantitative MRI analyses were performed using Dr. View/Linux software and a voxel-based specific regional analysis system. Significant correlations were observed between WMH, as well as MTA, and some executive function scores. Regression analysis revealed that MTA was the strongest predictor of flexibility and verbal fluency. These findings provide new insight into the relationship between quantitative MRI analyses and various types of executive dysfunction in elderly people with MCI due to AD and/or early phase AD. When cognitive function is examined in elderly patients with MCI due to AD or early phase AD, it is important to consider the involvement of WMH and MTA, which is indicative of AD pathology in cognitive dysfunction, particularly executive function.

    DOI: 10.14336/AD.2018.0929

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  31. Physiological Implications of Microglia-Synapse Interactions. International journal

    Hiroaki Wake, Hiroshi Horiuchi, Daisuke Kato, Andrew J Moorhouse, Junichi Nabekura

    Methods in molecular biology (Clifton, N.J.)   Vol. 2034   page: 69 - 80   2019

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    Microglia are the sole immune responding cells in the central nervous system. Their role as neuroimmune cells in the pathogenesis of various neurodegenerative and infectious diseases of the brain have been extensively studied. Upon brain disease and infection, they adopt an activated phenotype associated with the release of cytokines and neurotrophic factors and resulting in neuroprotective or neurotoxic outcomes. However, microglia are resident also in the healthy or physiological brain, but much less is known about their role(s) in the healthy brain, partly due to technical limitations regarding investigation of these highly reactive cells in the intact brain. Recent developments in molecular probes and in vivo optical imaging techniques has now helped to characterize microglia in the physiological or healthy brain. In vivo two-photon imaging of fluorescently labeled microglia have revealed that they are highly motile cells in the healthy brain, extending and retracting their processes that extend from a largely stationary cell soma. In this chapter, we briefly summarize some of the physiological functions of microglia in the uninjured brain, with a focus on interactions they have with synapses.

    DOI: 10.1007/978-1-4939-9658-2_6

    PubMed

  32. In Vivo Two-Photon Imaging of Microglial Synapse Contacts. International journal

    Daisuke Kato, Ako Ikegami, Hiroshi Horiuchi, Andrew J Moorhouse, Junichi Nabekura, Hiroaki Wake

    Methods in molecular biology (Clifton, N.J.)   Vol. 2034   page: 281 - 286   2019

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    Microglia are traditionally known as immune sentinels of the brain and as key player in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson disease, or amyotrophic lateral sclerosis. Recently, they were also identified as synaptic organizer, promoting formation and maturation of synapses as well as modifying synaptic activity. Interestingly, microglia-mediated synaptic pruning and microglia-mediated changes in synaptic plasticity were observed both during brain development and in neurodegenerative diseases, stressing the key role of microglia-synapse interaction in these processes. Here we descried a technique for noninvasive in vivo monitoring of microglia-synapse interactions by means of two-photon microscopy.

    DOI: 10.1007/978-1-4939-9658-2_20

    PubMed

  33. Activity-Dependent Myelination. International journal

    Daisuke Kato, Hiroaki Wake

    Advances in experimental medicine and biology   Vol. 1190   page: 43 - 51   2019

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    Oligodendrocyte form myelin around the axons to regulate the conduction velocity. Myelinated axons are composed of white matter to act as cables to connect distinct brain regions. Recent human MRI studies showed that the signal from white matter change in the people with special skills such as taxi driver, piano player, and juggling. The change of the white matter suggested that (1) The plasticity of myelination depends on neuronal activity (activity-dependent myelination) and (2) White matter plasticity is essential for brain functions. In this session, we discussed that how the un-electrical components, oligodendrocytes, and its precursor cells receive the signal from electrically active neurons and differentiate, proliferate, and myelinate the axons to modulate the activity of neuronal circuits, ultimately affect on their behaviors. In this review, we highlight the physiological functions of oligodendrocyte and their neuronal activity-dependent functions and thus show new insight for their contribution to brain functions.

    DOI: 10.1007/978-981-32-9636-7_4

    PubMed

  34. Microglia Enhance Synapse Activity to Promote Local Network Synchronization

    Ryohei Akiyoshi, Hiroaki Wake, Daisuke Kato, Hiroshi Horiuchi, Riho Ono, Ako Ikegami, Koichiro Haruwaka, Toshiaki Omori, Yoshihisa Tachibana, Andrew J. Moorhouse, Junichi Nabekura

    eneuro   Vol. 5 ( 5 ) page: ENEURO.0088 - 18.2018   2018.9

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    DOI: 10.1523/ENEURO.0088-18.2018

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  35. Activity-dependent functions of non-electrical glial cells. International journal

    Daisuke Kato, Kei Eto, Junichi Nabekura, Hiroaki Wake

    Journal of biochemistry   Vol. 163 ( 6 ) page: 457 - 464   2018.6

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    Electrical activity is essential for brain function. However, neurons, the electrically active cells, are less numerous than the non-electrical glial cells in the central nervous system. The non-electrical components modify the function of neural circuits, depending on the electrical neuronal activity, by wrapping synapses, myelinating axons and phagocytozing the neuronal components. Moreover, recent evidence has suggested that they contribute to neurological and psychiatric disease by regulating neuronal circuits, ultimately affecting their behaviour. In this review, we highlight the physiological functions of glial cells, particularly the electrical activity-dependent processes, to provide further insight into their role in brain function.

    DOI: 10.1093/jb/mvy023

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  36. Stiripentol for the treatment of super-refractory status epilepticus with cross-sensitivity

    Y. Uchida, K. Terada, Y. Madokoro, T. Fujioka, M. Mizuno, T. Toyoda, D. Kato, N. Matsukawa

    Acta Neurologica Scandinavica   Vol. 137 ( 4 ) page: 432 - 437   2018.4

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    Authorship:Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Wiley  

    DOI: 10.1111/ane.12888

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  37. Failure to improve after ovarian resection could be a marker of recurrent ovarian teratoma in anti-NMDAR encephalitis: a case report. Invited Reviewed

    Uchida Y, Kato D, Yamashita Y, Ozaki Y, Matsukawa N.

    Neuropsychiatr Dis Treat     2018.1

  38. Passively acquired thyroid autoantibodies from intravenous immunoglobulin in autoimmune encephalitis: Two case reports. International journal

    Yuto Uchida, Daisuke Kato, Kenichi Adachi, Takanari Toyoda, Noriyuki Matsukawa

    Journal of the neurological sciences   Vol. 383   page: 116 - 117   2017.12

  39. Utility of T1- and T2-Weighted High-Resolution Vessel Wall Imaging for the Diagnosis and Follow Up of Isolated Posterior Inferior Cerebellar Artery Dissection with Ischemic Stroke: Report of 4 Cases and Review of the Literature. International journal

    Yuta Madokoro, Keita Sakurai, Daisuke Kato, Yuko Kondo, Masahiro Oomura, Noriyuki Matsukawa

    Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association   Vol. 26 ( 11 ) page: 2645 - 2651   2017.11

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    BACKGROUND: An accurate diagnosis of isolated posterior inferior cerebellar artery dissection (iPICA-D) is difficult due to the limitation of spatial resolution on conventional magnetic resonance imaging (MRI) techniques to detect subtle vessel wall abnormalities. The recent development of MRI techniques, including high-resolution vessel wall imaging (HRVWI), has resulted in the improved diagnostic accuracy and efficiency of iPICA-D. In fact, T1-weighted HRVWI, which can reveal intramural hematomas in the posterior inferior cerebellar artery (PICA), is useful for the diagnosis of iPICA-D. However, the utility of T2-weighted HRVWI has not been previously reported. The aim of this study was to investigate the diagnostic utility of T1- and T2-weighted HRVWI for the diagnosis of iPICA-D. METHODS: We retrospectively evaluated MRI findings including intramural hematomas, dilations, and chronological changes in 4 patients with iPICA-D admitted to our hospital and related facility from January 2015 to August 2016. In addition to T1-weighted HRVWI, T2-weighted HRVWI was performed on isovoxel three-dimensional (3D) fast spin-echo or 3D sampling perfection with application-optimized contrast using different flip-angle evolution. We also reviewed cases of nonhemorrhagic iPICA-D with ischemic onset in which the MRI findings were described. RESULTS: In all 4 patients, in addition to the intramural hematomas on T1-weighted HRVWI, T2-weighted HRVWI clearly showed the fusiform dilation of the external diameter of the PICA. T2-weighted HRVWI was more useful than other techniques, including T1-weighted HRVWI, for the evaluation of arterial shape changes. CONCLUSIONS: Like T1-weighted HRVWI, T2-weighted HRVWI is useful for the diagnosis and assessment of chronological changes in vessel wall abnormalities during the follow-up period.

    DOI: 10.1016/j.jstrokecerebrovasdis.2017.06.038

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  40. Hippocampal Cholinergic Neurostimulating Peptide as a Possible Modulating Factor against Glutamatergic Neuronal Disability by Amyloid Oligomers. International journal

    Toyohiro Sato, Yoshiaki Ohi, Daisuke Kato, Masayuki Mizuno, Hiroshi Takase, Tetsuko Kanamori, Cesar V Borlongan, Akira Haji, Noriyuki Matsukawa

    Cell transplantation   Vol. 26 ( 9 ) page: 1542 - 1550   2017.9

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    Despite having pathological changes in the brain associated with Alzheimer's disease (AD), some patients have preserved cognitive function. A recent epidemiological study has shown that diet, exercise, cognitive training, and vascular risk monitoring interventions may reduce cognitive decline in at-risk elderly people in the general population. However, the details of molecular mechanisms underlying this cognitive function preservation are still unknown. Previous reports have demonstrated that enriched environments prevent the impairment of hippocampal long-term potentiation (LTP) through β2-adrenergic signals, when LTP is incompletely suppressed by synthetic amyloid-β (Aβ) oligomers. The cholinergic network from the medial septal nucleus (MSN) is also a main modulating system for hippocampal glutamatergic neural activation through nicotinergic and/or muscarinergic acetylcholine receptors. Previously, we reported the importance of a cholinergic regulator gene in the MSN, hippocampal cholinergic neurostimulating peptide (HCNP). By using hippocampal sections from mice, we here demonstrated that the cholinergic neural activation from the MSN enhanced the glutamatergic neuronal activity during unsaturated LTP but not during saturated LTP. Synthetic Aβ oligomers suppressed the hippocampal glutamatergic activity in a concentration-dependent manner. Furthermore, HCNP, as well as a cholinergic agonist acting through the muscarinic M1 receptor, prevented the suppression of hippocampal glutamatergic neuronal activity induced by synthetic Aβ oligomers. This result suggests that the persisting cholinergic activation might be a potential explanation for the individual differences in cognitive effects of AD pathological changes.

    DOI: 10.1177/0963689717721232

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  41. Paranodal dissection in chronic inflammatory demyelinating polyneuropathy with anti-neurofascin-155 and anti-contactin-1 antibodies. International journal

    Haruki Koike, Masato Kadoya, Ken-Ichi Kaida, Shohei Ikeda, Yuichi Kawagashira, Masahiro Iijima, Daisuke Kato, Hidenori Ogata, Ryo Yamasaki, Noriyuki Matsukawa, Jun-Ichi Kira, Masahisa Katsuno, Gen Sobue

    Journal of neurology, neurosurgery, and psychiatry   Vol. 88 ( 6 ) page: 465 - 473   2017.6

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    OBJECTIVE: To investigate the morphological features of chronic inflammatory demyelinating polyneuropathy (CIDP) with autoantibodies directed against paranodal junctional molecules, particularly focusing on the fine structures of the paranodes. METHODS: We assessed sural nerve biopsy specimens obtained from 9 patients with CIDP with anti-neurofascin-155 antibodies and 1 patient with anti-contactin-1 antibodies. 13 patients with CIDP without these antibodies were also examined to compare pathological findings. RESULTS: Characteristic light and electron microscopy findings in transverse sections from patients with anti-neurofascin-155 and anti-contactin-1 antibodies indicated a slight reduction in myelinated fibre density, with scattered myelin ovoids, and the absence of macrophage-mediated demyelination or onion bulbs. Teased-fibre preparations revealed that segmental demyelination tended to be found in patients with relatively higher frequencies of axonal degeneration and was tandemly found at consecutive nodes of Ranvier in a single fibre. Assessment of longitudinal sections by electron microscopy revealed that detachment of terminal myelin loops from the axolemma was frequently found at the paranode in patients with anti-neurofascin-155 and anti-contactin-1 antibody-positive CIDP compared with patients with antibody-negative CIDP. Patients with anti-neurofascin-155 antibodies showed a positive correlation between the frequencies of axo-glial detachment at the paranode and axonal degeneration, as assessed by teased-fibre preparations (p<0.05). CONCLUSIONS: Paranodal dissection without classical macrophage-mediated demyelination is the characteristic feature of patients with CIDP with autoantibodies to paranodal axo-glial junctional molecules.

    DOI: 10.1136/jnnp-2016-314895

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  42. Fatal remote cerebral hemorrhage at a site of a microbleed immediately after intravenous thrombolysis Invited Reviewed

    Oomura M, Fujioka T, Uchida Y, Kato D, Nishikawa Y, Matsukawa N

        2017.4

  43. Combination of ketogenic diet and stiripentol for super-refractory status epilepticus: A case report. International journal

    Yuto Uchida, Daisuke Kato, Takanari Toyoda, Masahiro Oomura, Yoshino Ueki, Kenji Ohkita, Noriyuki Matsukawa

    Journal of the neurological sciences   Vol. 373   page: 35 - 37   2017.2

  44. Retropharyngeal calcific tendinitis presenting with neck pain and severe dysphagia: A case report. Invited Reviewed

    Madokoro Y, Mizuno M, Kato D, Toyoda T, Ohkita K, Matsukawa N

    Neurology and Clinical Neuroscience     2016.12

  45. [Frontiers in Live Bone Imaging Researches. In vivo imaging of neuron and glia].

    Hiroaki Wake, Daisuke Kato

    Clinical calcium   Vol. 25 ( 6 ) page: 859 - 70   2015.6

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    Glial cells originate the Greek word'glue'had traditionally been only thought as supporting cells for neurons. Because glial cells are electrically non-excitable, neuroscience researchers have focused on elucidation of excitable cell properties, neuron. Recent advanced optical methods lead us to observe glial structure, motility and their function in normal physiological conditions. These approaches let us to know that they are not just the supporting cells for neuron but could receive signal from neurons through receptors for neurotransmitters and to regulate neuronal functions, thus modulating behavior phenotype. Such studies also suggest that glial cells are highly dynamic and actively maintain brain homeostasis. Here, we review physiological function of glial cells through a new perspective clarified by innovations of imaging technology including two-photon microscope.

    PubMed

  46. Enhancement of long-term potentiation via muscarinic modulation in the hippocampus of HCNP precursor transgenic mice Invited Reviewed

    Neurosci Lett.     2015.4

  47. [Brain function and white matter].

    Hiroaki Wake, Daisuke Kato

    Brain and nerve = Shinkei kenkyu no shinpo   Vol. 67 ( 4 ) page: 505 - 12   2015.4

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    Accumulated evidence shows that neural information processing takes place in superficial layers of the brain called the gray matter. Synapses, which connect different neurons reside in the gray matter and are considered the major components of information processing and plasticity. On the other hand, myelinated axons lie beneath the gray matter. These bundles of cables connect neurons in the different brain regions to form functional neural circuits. Myelinated axons were of little of interest to neuroscientists and have long been ignored in the formation of functional neuronal circuits. Recent evidence shows that myelin formed by oligodendrocytes shows plastic changes depending on neuronal activity. In this issue, we discuss the plastic changes of myelin and its functional role in learning and training.

    DOI: 10.11477/mf.1416200167

    PubMed

  48. Phosphorylation of collapsin response mediator protein-2 regulates its localization and association with hippocampal cholinergic neurostimulating peptide precursor in the hippocampus Invited Reviewed

    Mizuno M, Kato D, Kanamori T, Toyoda T, Suzuki T, Ojika K, Matsukawa N

    Neurosci Lett.     2013.2

  49. Co-localization of hippocampal cholinergic neurostimulating peptide precursor with collapsin response mediator protein-2 at presynaptic terminals in hippocampus Invited Reviewed

    Kato D, Mitake S, Mizuno M, Kanamori T, Suzuki T, Ojika K, Matsukawa N

    Neurosci Lett.     2012.5

  50. Suppression of astrocyte lineage in adult hippocampal progenitor cells expressing hippocampal cholinergic neurostimulating peptide precursor in an in vivo ischemic model Invited Reviewed

    Toyoda T, Matsukawa N, Sagisaka T, Uematsu N, Kanamori T, Kato D, Mizuno M, Wake H, Hida H, Borlongan CV, Ojika K

    Cell Transplant.     2012

  51. Utility of the fluid-attenuated inversion recovery sequence in detecting a hyperintense putaminal rim in multiple system atrophy-parkinsonism: a preliminary study Invited Reviewed

    Sakurai K, Yamawaki T, Okita K, Kato D, Matsukawa N, Kawaguchi T, Kobayashi S, Nagai K, Muto M, Hosono A, Shibamoto Y

    Eur Neurol.     2011

  52. Utility of the fluid-attenuated inversion recovery sequence in detecting a hyperintense putaminal rim in multiple system atrophy-parkinsonism: a preliminary study. International journal

    Keita Sakurai, Takemori Yamawaki, Kenji Okita, Daisuke Kato, Noriyuki Matsukawa, Takatsune Kawaguchi, Susumu Kobayashi, Keiichi Nagai, Masahiro Muto, Akihiro Hosono, Yuta Shibamoto

    European neurology   Vol. 66 ( 1 ) page: 42 - 6   2011

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    OBJECTIVE: To investigate the utility of fluid-attenuated inversion recovery (FLAIR) imaging for diagnosing multiple system atrophy-parkinsonism (MSA-P). METHODS: We retrospectively evaluated 49 subjects (19 with MSA-P including 11 with early-stage disease, 15 with Parkinson's disease and 15 matched controls) in order to compare the diagnostic value of FLAIR imaging to detect a hyperintense putaminal rim (HPR) with that of T(2)-weighted (T2W) imaging. RESULTS: Compared with T2W imaging, FLAIR imaging detected HPR more conspicuously in the 19 MSA-P patients (p = 0.01); this trend was also observed in 11 early-stage MSA-P patients (p = 0.01). Furthermore, FLAIR imaging tended to increase sensitivity of detecting HPR compared with T2W imaging (all patients: 89 vs. 58%, p = 0.07; early-stage patients: 100 vs. 55%, p = 0.06). CONCLUSIONS: FLAIR imaging might be more useful for detecting HPR in MSA-P patients, even though they are at an early stage.

    DOI: 10.1159/000328674

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  53. Suppressed phosphorylation of collapsin response mediator protein-2 in the hippocampus of HCNP precursor transgenic mice Invited Reviewed

    Kanamori T, Matsukawa N, Kobayashi H, Uematsu N, Sagisaka T, Toyoda T, Kato D, Oikawa S, Ojika K

    Brain Res.     2010.10

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Books 7

  1. 脳の半分を占めるグリア細胞 神経活動依存的な髄鞘化の障害がもたらす神経回路変容

    加藤大輔、和氣弘明

    実験医学 羊土社  2019.11 

  2. 臓器連環による生体恒常性の破綻と疾患/グリア細胞が担う脳神経回路の動的恒常性

    和氣弘明、加藤大輔( Role: Joint author)

    実験医学  2019.4 

  3. アルツハイマー病発症メカニズムと新規診断法創薬治療開発 第2節ミクログリア異常によるアルツハイマー病発症メカニズム

    和氣弘明、加藤大輔

    エヌ・ティー・エス  2018.8 

  4. 脳神経回路と高次脳機能 スクラップ&ビルドによる心の発達と脳疾患の謎を解く/グリア細胞による神経回路のスクラップアンドビルド

    和氣弘明、加藤大輔

    実験医学 羊土社  2018.7 

  5. 特集:骨の生体イメージング/最前線 神経・グリア細胞の生体イメージング

    和氣弘明、加藤大輔

    CLINICALCALCIUM 医薬ジャーナル社  2015.6 

  6. 増大特集 大脳皮質 vs. 大脳白質 白質と脳機能 BRAIN and NERVE-神経研究の進歩

    和氣弘明、加藤大輔

    医学書院  2015.4 

  7. グリア細胞が心を動かす/神経活動に依存した髄鞘化

    和氣弘明、加藤大輔、R. Douglas Fields

    実験医学 羊土社  2013.7 

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Presentations 1

  1. 神経精神疾患の病態解明へ向けた臨床的特徴を抽出し、基礎研究へつなげるための融合研究とその育成

    加藤大輔

    第127回日本解剖学会総会・全国学術集会  2022.3.27  日本解剖学会

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    Event date: 2022.3

    Presentation type:Symposium, workshop panel (public)  

Research Project for Joint Research, Competitive Funding, etc. 4

  1. 新規光刺激技術を用いた脳領域間における神経細胞活動の可視化と操作法の開発

    2022.2 - 2024.1

  2. 幻覚発症メカニズムに焦点を当てたレビー小体型認知症の病態解明

    2021.4 - 2022.3

  3. 脳内の可塑的な脂質変化に焦点を当てたアルツハイマー型認知症に対する新規治療法の開発に関する研究

    2021.3 - 2022.3

  4. 髄鞘化の光制御による認知症病態解明

    2020.8 - 2022.8

KAKENHI (Grants-in-Aid for Scientific Research) 7

  1. 髄鞘がもつ多面的機能の理解に基づく神経精神疾患の病態解明

    Grant number:21466081  2022.4 - 2026.3

    科学技術振興機構(JST)  創発的研究支援事業 

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    Grant amount:\20000000

  2. 脳領域間の神経細胞活動から発せられる揺らぎによる高次脳機能の透視

    Grant number:21H05587  2021.10 - 2023.3

    学術変革領域研究(A) 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\9730000 ( Direct Cost: \8500000 、 Indirect Cost:\1230000 )

  3. 血液脳関門の破綻に着目した術後神経認知機能障害の発症機序解明

    Grant number:21H03025  2021.4 - 2025.3

    科学研究費助成事業  基盤研究(B)

    祖父江 和哉, 志田 恭子, 加藤 大輔, 小山内 実, 大澤 匡弘, 中西 俊之, 仙頭 佳起, 打田 佑人

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    Authorship:Coinvestigator(s) 

    麻酔・手術後の神経認知機能障害(neurocognitive disorder: NCD)を、発症機序まで突き止めた研究はない。本研究では、マウスの術後NCDモデルで、中枢神経機能を維持する血液脳関門(BBB)の破綻を確認し、神経活動の障害との関連を明らかにする。また、脳内炎症等に関与するミクログリアに着目し、BBBの破綻の発生機序を検討する。さらに、申請者らが開発したヒトのMRIによるBBB機能評価法を用いて、術後NCD患者のBBBの破綻を確認する。
    以上より、術後NCDの発症機序を明らかにし、周術期管理のリスク因子を検討して、高齢化で問題性が高まる術後NCDの予防や治療法の開発に貢献する。

  4. 神経回路基盤の網羅的解析による神経・精神疾患に対する創薬技術向上を目指した評価系の構築

    Grant number:20ak0101150h0001  2020.12 - 2023.3

    国立研究開発法人日本医療研究開発機構  創薬基盤推進研究事業 

    加藤大輔

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    Authorship:Principal investigator 

  5. 感覚モダリティ理解のためのミクログリア・シナプス接触の多角的解析

    Grant number:20KK0170  2020.10 - 2024.3

    日本学術振興会  科学研究費助成事業 国際共同研究加速基金(国際共同研究強化(B))  国際共同研究加速基金(国際共同研究強化(B))

    和氣 弘明

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    Authorship:Coinvestigator(s) 

    本国際研究では中枢神経系唯一の免疫細胞であるミクログリアに着目し、ミクログリアがシナプスの構造的・機能的可塑性を修飾する背景を踏まえ、多角的階層的な技術を相互補完することによって、ミクログリアのシナプスに対する時間的(発達・成熟)および空間(脳領域)特異的な生理機能を明らかにする。さらにこれを異種感覚の可塑的変化のメカニズムに繋げ、そこから精神病態を考察する。

  6. 白質機能制御に焦点を当てたアルツハイマー型認知症に対する治療法開発

    Grant number:20K16574  2020.4 - 2022.3

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    加藤 大輔

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    近年、頭部MRIで描出される白質病変がアルツハイマー型認知症(AD)では、認知症発症前から出現し、認知機能低下を促進させることが判明した。しかしながらその詳細な機序は不明である。白質は髄鞘化された軸索で構成され、これまで研究代表者はこの髄鞘に着目し、神経活動依存的な髄鞘化が障害された際の学習障害とその背景にある神経回路基盤を解明してきた。そこで本研究では、髄鞘を形成するオリゴデンドロサイトとその前駆細胞が示す機能応答の生理学的特性を解明することでADでの変化を抽出後、この機能応答の障害が白質機能低下及び学習障害を引き起こすか検証し、さらに機能応答に関わる分子機構を同定することを目的とする。

  7. The effect of activity dependent myelination on to the neuronal circuit activity

    Grant number:26710004  2014.4 - 2018.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (A)  Grant-in-Aid for Young Scientists (A)

    WAKE Hiroaki, KATO Daisuke, AKIYOSHI Ryohei

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    Myelination increases conduction velocity and promotes brain functions. Myelin dysregulation is frequently associated with learning and cognition deficits, ultimately causing neurological and psychiatric disorders. However, it has not been revealed what perturbation of neural activity induced by myelin dysregulation impairs learning. Here, we measured neural activity in the motor cortex during motor learning in transgenic mice with a subtle impairment of their myelin regulation.This myelin dysregulation impaired motor learning and was accompanied by a decrease in the amplitude of movement-related activity, an increase in the frequency of spontaneous activity, and a widening in the timing of cortical responses to thalamic stimulation. Repetitive pairing of forelimb movements with optogenetic stimulation of thalamocortical axon terminals partially restored learning.

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Teaching Experience (On-campus) 6

  1. 肉眼解剖学

    2021

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    授業と実習

  2. 基礎医学実習

    2021

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    授業と実習

  3. 神経解剖学

    2021

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    授業と実習

  4. 基礎医学実習

    2020

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    研究室での基礎配属学生への指導

  5. 肉眼解剖学

    2020

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    肉眼解剖学・骨学の実習

  6. 神経解剖学

    2020

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    神経解剖学授業と実習

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Teaching Experience (Off-campus) 2

  1. 神経内科講義

    2021.4 Nagoya City University)

  2. 神経内科講義

    2020.4 Nagoya City University)

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    Level:Undergraduate (specialized)  Country:Japan

 

Media Coverage 4

  1. 母体の免疫活性が胎児ミクログリアの動態に持続的な変化を引き起こすことを発見  ― 発達障害や統合失調症への関連を示唆 ―

    神戸大学  2020.12

  2. 痛みを感じた時の脳内の神経回路変化をホログラフィック顕微鏡によって解明

    AMED 名古屋大学  2020.3

  3. 精神・神経変性疾患の治療に朗報! ~脳内の免疫細胞であるミクログリアが血液脳関門の機能を制御することを発見~

    名古屋大学 神戸大学  2019.12

  4. 学習障害を引き起こす髄鞘機能障害の神経回路活動を解明

    神戸大学 生理学研究所  2019.9

Academic Activities 2

  1. 極みプロジェクト会議

    Role(s):Panel moderator, session chair, etc.

    2021.3

  2. 極みプロジェクト会議

    Role(s):Panel moderator, session chair, etc.

    和氣弘明  2020.9