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  1. Article ; Online: Developmental synapse remodeling in the cerebellum and visual thalamus [version 1; peer review

    Masanobu Kano / Takaki Watanabe

    F1000Research, Vol

    2 approved]

    2019  Volume 8

    Abstract: Functional neural circuits of mature animals are shaped during postnatal development by eliminating early-formed redundant synapses and strengthening of necessary connections. In the nervous system of newborn animals, redundant synapses are only ... ...

    Abstract Functional neural circuits of mature animals are shaped during postnatal development by eliminating early-formed redundant synapses and strengthening of necessary connections. In the nervous system of newborn animals, redundant synapses are only transient features of the circuit. During subsequent postnatal development, some synapses are strengthened whereas other redundant connections are weakened and eventually eliminated. In this review, we introduce recent studies on the mechanisms of developmental remodeling of climbing fiber–to–Purkinje cell synapses in the cerebellum and synapses from the retina to neurons in the dorsal lateral geniculate nucleus of the visual thalamus (retinogeniculate synapses). These are the two representative models of developmental synapse remodeling in the brain and they share basic principles, including dependency on neural activity. However, recent studies have disclosed that, in several respects, the two models use different molecules and strategies to establish mature synaptic connectivity. We describe similarities and differences between the two models and discuss remaining issues to be tackled in the future in order to understand the general schemes of developmental synapse remodeling.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2019-07-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Combining electrophysiology and optogenetics for functional screening of pyramidal neurons in the mouse prefrontal cortex

    Kenichiro Nagahama / Shuhei Fujino / Takaki Watanabe / Naofumi Uesaka / Masanobu Kano

    STAR Protocols, Vol 2, Iss 2, Pp 100469- (2021)

    2021  

    Abstract: Summary: Here, we present a comprehensive protocol to analyze the roles of disease-related genes in synaptic transmission. We have developed a pipeline of electrophysiological techniques and combined these with optogenetics in the medial prefrontal ... ...

    Abstract Summary: Here, we present a comprehensive protocol to analyze the roles of disease-related genes in synaptic transmission. We have developed a pipeline of electrophysiological techniques and combined these with optogenetics in the medial prefrontal cortex of mice. This methodology provides a cost-effective, faster, and easier screening approach to elucidate functional aspects of single genes in several regions in the mouse brain such as a specific layer of the mPFC.For complete details on the use and execution of this protocol, please refer to Nagahama et al. (2020) and Sacai et al. (2020).
    Keywords High Throughput Screening ; Microscopy ; Neuroscience ; Science (General) ; Q1-390
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Type-1 metabotropic glutamate receptor signaling in cerebellar Purkinje cells in health and disease [version 1; referees

    Masanobu Kano / Takaki Watanabe

    F1000Research, Vol

    3 approved]

    2017  Volume 6

    Abstract: The cerebellum is a brain structure involved in coordination, control, and learning of movements, as well as certain aspects of cognitive function. Purkinje cells are the sole output neurons from the cerebellar cortex and therefore play crucial roles in ... ...

    Abstract The cerebellum is a brain structure involved in coordination, control, and learning of movements, as well as certain aspects of cognitive function. Purkinje cells are the sole output neurons from the cerebellar cortex and therefore play crucial roles in the overall function of the cerebellum. The type-1 metabotropic glutamate receptor (mGluR1) is a key “hub” molecule that is critically involved in the regulation of synaptic wiring, excitability, synaptic response, and synaptic plasticity of Purkinje cells. In this review, we aim to highlight how mGluR1 controls these events in Purkinje cells. We also describe emerging evidence that altered mGluR1 signaling in Purkinje cells underlies cerebellar dysfunctions in several clinically relevant mouse models of human ataxias.
    Keywords Animal Genetics ; Behavioral Neuroscience ; Medical Genetics ; Motor Systems ; Movement Disorders ; Neurobiology of Disease & Regeneration ; Neurodevelopment ; Neurogenetics ; Neuronal Signaling Mechanisms ; Neuropharmacology & Psychopharmacology ; Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2017-04-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: mGluR5 Is Substitutable for mGluR1 in Cerebellar Purkinje Cells for Motor Coordination, Developmental Synapse Elimination, and Motor Learning

    Maria Harbers / Harumi Nakao / Takaki Watanabe / Kyoko Matsuyama / Shoichi Tohyama / Kazuki Nakao / Yasushi Kishimoto / Masanobu Kano / Atsu Aiba

    Cells, Vol 11, Iss 2004, p

    2022  Volume 2004

    Abstract: Group I metabotropic glutamate receptors (mGluRs) include mGluR1 and mGluR5, which are coupled to the Gq family of heterotrimeric G-proteins and readily activated by their selective agonist 3,5-dihydroxyphenilglycine (DHPG). mGluR1 and mGluR5 exhibit ... ...

    Abstract Group I metabotropic glutamate receptors (mGluRs) include mGluR1 and mGluR5, which are coupled to the Gq family of heterotrimeric G-proteins and readily activated by their selective agonist 3,5-dihydroxyphenilglycine (DHPG). mGluR1 and mGluR5 exhibit nearly complementary distributions spatially or temporally in the central nervous system (CNS). In adult cerebellar Purkinje cells (PCs), mGluR1 is a dominant group I mGluR and mGluR5 is undetectable. mGluR1 expression increases substantially during the first three weeks of postnatal development and remains high throughout adulthood. On the other hand, mGluR5 expression is observed during the first two postnatal weeks and then decreases. However, functional differences between mGluR1 and mGluR5 in the CNS remains to be elucidated. To address this issue, we generated “mGluR5-rescue” mice in which mGluR5 is specifically expressed in PCs in global mGluR1-knockout (KO) mice. mGluR5-rescue mice exhibited apparently normal motor coordination, developmental elimination of redundant climbing fiber (CF)-PC synapses, and delay eyeblink conditioning, which were severely impaired in mGluR1-KO mice. We concluded that mGluR5 is functionally comparable with mGluR1 in cerebellar PCs.
    Keywords Purkinje cells ; mGluR5 ; mGluR1 ; motor coordination ; synapse elimination ; eyeblink conditioning ; Biology (General) ; QH301-705.5
    Subject code 572
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Autism spectrum disorder-like behavior caused by reduced excitatory synaptic transmission in pyramidal neurons of mouse prefrontal cortex

    Hiroaki Sacai / Kazuto Sakoori / Kohtarou Konno / Kenichiro Nagahama / Honoka Suzuki / Takaki Watanabe / Masahiko Watanabe / Naofumi Uesaka / Masanobu Kano

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 15

    Abstract: CNTNAP2 or AHI1 are autism-associated genes. Here the authors show using knockdown of the genes that this results in reduced excitatory synaptic transmission in layer 2/3 pyramidal neurons in the prefrontal cortex and is associated with impaired social ... ...

    Abstract CNTNAP2 or AHI1 are autism-associated genes. Here the authors show using knockdown of the genes that this results in reduced excitatory synaptic transmission in layer 2/3 pyramidal neurons in the prefrontal cortex and is associated with impaired social interaction in mice.
    Keywords Science ; Q
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: AUTS2 Governs Cerebellar Development, Purkinje Cell Maturation, Motor Function and Social Communication

    Kunihiko Yamashiro / Kei Hori / Esther S.K. Lai / Ryo Aoki / Kazumi Shimaoka / Nariko Arimura / Saki F. Egusa / Asami Sakamoto / Manabu Abe / Kenji Sakimura / Takaki Watanabe / Naofumi Uesaka / Masanobu Kano / Mikio Hoshino

    iScience, Vol 23, Iss 12, Pp 101820- (2020)

    2020  

    Abstract: Summary: Autism susceptibility candidate 2 (AUTS2), a risk gene for autism spectrum disorders (ASDs), is implicated in telencephalon development. Because AUTS2 is also expressed in the cerebellum where defects have been linked to ASDs, we investigated ... ...

    Abstract Summary: Autism susceptibility candidate 2 (AUTS2), a risk gene for autism spectrum disorders (ASDs), is implicated in telencephalon development. Because AUTS2 is also expressed in the cerebellum where defects have been linked to ASDs, we investigated AUTS2 functions in the cerebellum. AUTS2 is specifically localized in Purkinje cells (PCs) and Golgi cells during postnatal development. Auts2 conditional knockout (cKO) mice exhibited smaller and deformed cerebella containing immature-shaped PCs with reduced expression of Cacna1a. Auts2 cKO and knock-down experiments implicated AUTS2 participation in elimination and translocation of climbing fiber synapses and restriction of parallel fiber synapse numbers. Auts2 cKO mice exhibited behavioral impairments in motor learning and vocal communications. Because Cacna1a is known to regulate synapse development in PCs, it suggests that AUTS2 is required for PC maturation to elicit normal development of PC synapses and thus the impairment of AUTS2 may cause cerebellar dysfunction related to psychiatric illnesses such as ASDs.
    Keywords Molecular Neuroscience ; Developmental Neuroscience ; Cellular Neuroscience ; Science ; Q
    Language English
    Publishing date 2020-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Combined glyoxalase 1 dysfunction and vitamin B6 deficiency in a schizophrenia model system causes mitochondrial dysfunction in the prefrontal cortex

    Kazuya Toriumi / Stefano Berto / Shin Koike / Noriyoshi Usui / Takashi Dan / Kazuhiro Suzuki / Mitsuhiro Miyashita / Yasue Horiuchi / Akane Yoshikawa / Mai Asakura / Kenichiro Nagahama / Hsiao-Chun Lin / Yuki Sugaya / Takaki Watanabe / Masanobu Kano / Yuki Ogasawara / Toshio Miyata / Masanari Itokawa / Genevieve Konopka /
    Makoto Arai

    Redox Biology, Vol 45, Iss , Pp 102057- (2021)

    2021  

    Abstract: Methylglyoxal (MG) is a reactive and cytotoxic α-dicarbonyl byproduct of glycolysis. Our bodies have several bio-defense systems to detoxify MG, including an enzymatic system by glyoxalase (GLO) 1 and GLO2. We identified a subtype of schizophrenia ... ...

    Abstract Methylglyoxal (MG) is a reactive and cytotoxic α-dicarbonyl byproduct of glycolysis. Our bodies have several bio-defense systems to detoxify MG, including an enzymatic system by glyoxalase (GLO) 1 and GLO2. We identified a subtype of schizophrenia patients with novel mutations in the GLO1 gene that results in reductions of enzymatic activity. Moreover, we found that vitamin B6 (VB6) levels in peripheral blood of the schizophrenia patients with GLO1 dysfunction are significantly lower than that of healthy controls. However, the effects of GLO1 dysfunction and VB6 deficiency on the pathophysiology of schizophrenia remains poorly understood. Here, we generated a novel mouse model for this subgroup of schizophrenia patients by feeding Glo1 knockout mice VB6-deficent diets (KO/VB6(−)) and evaluated the combined effects of GLO1 dysfunction and VB6 deficiency on brain function. KO/VB6(−) mice accumulated homocysteine in plasma and MG in the prefrontal cortex (PFC), hippocampus, and striatum, and displayed behavioral deficits, such as impairments of social interaction and cognitive memory and a sensorimotor deficit in the prepulse inhibition test. Furthermore, we found aberrant gene expression related to mitochondria function in the PFC of the KO/VB6(−) mice by RNA-sequencing and weighted gene co-expression network analysis (WGCNA). Finally, we demonstrated abnormal mitochondrial respiratory function and subsequently enhanced oxidative stress in the PFC of KO/VB6(−) mice in the PFC. These findings suggest that the combination of GLO1 dysfunction and VB6 deficiency may cause the observed behavioral deficits via mitochondrial dysfunction and oxidative stress in the PFC.
    Keywords Glyoxalase 1 ; Vitamin B6 ; Methylglyoxal ; Schizophrenia ; Mitochondria ; Oxidative stress ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 572
    Language English
    Publishing date 2021-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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