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  • 1
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 34, No. 4 ( 2014-01-22), p. 1115-1126
    Abstract: The hippocampus plays important roles in brain functions. Despite the importance of hippocampal functions, recent analyses of neuronal migration have mainly been performed on the cerebral neocortex, and the cellular mechanisms responsible for the formation of the hippocampus are not yet completely understood. Moreover, why a prolonged time is required for hippocampal neurons to complete their migration has been unexplainable for several decades. We analyzed the migratory profile of neurons in the developing mouse hippocampal CA1 region and found that the hippocampal pyramidal neurons generated near the ventricle became postmitotic multipolar cells and accumulated in the multipolar cell accumulation zone (MAZ) in the late stage of development. The hippocampal neurons passed through the pyramidal layer by a unique mode of migration. Their leading processes were highly branched and made contact with many radial fibers. Time-lapse imaging revealed that the migrating cells changed their scaffolds from the original radial fibers to other radial fibers, and as a result they proceed in a zigzag manner, with long intervals. The migrating cells in the hippocampus reminded us of “rock climbers” that instead of using their hands to pull up their bodies were using their leading processes to pull up their cell bodies. Because this mode of migration had never been described, we called it the “climbing” mode. The change from the “climbing” mode in the hippocampus to the “locomotion” mode in the neocortex may have contributed to the brain expansion during evolution.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2014
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Society for Neuroscience ; 2012
    In:  The Journal of Neuroscience Vol. 32, No. 45 ( 2012-11-07), p. 16031-16039
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 32, No. 45 ( 2012-11-07), p. 16031-16039
    Abstract: We often have to make risky decisions between alternatives with outcomes that can be better or worse than the outcomes of safer alternatives. Although previous studies have implicated various brain regions in risky decision making, it remains unknown which regions are crucial for balancing whether to take a risk or play it safe. Here, we focused on the anterior insular cortex (AIC), the causal involvement of which in risky decision making is still unclear, although human imaging studies have reported AIC activation in various gambling tasks. We investigated the effects of temporarily inactivating the AIC on rats' risk preference in two types of gambling tasks, one in which risk arose in reward amount and one in which it arose in reward delay. As a control within the same subjects, we inactivated the adjacent orbitofrontal cortex (OFC), which is well known to affect risk preference. In both gambling tasks, AIC inactivation decreased risk preference whereas OFC inactivation increased it. In risk-free control situations, AIC and OFC inactivations did not affect decision making. These results suggest that the AIC is causally involved in risky decision making and promotes risk taking. The AIC and OFC may be crucial for the opposing motives of whether to take a risk or avoid it.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2012
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 3
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 30, No. 33 ( 2010-08-18), p. 10953-10966
    Abstract: Neurons in the developing mammalian neocortex form the cortical plate (CP) in an “inside-out” manner; that is, earlier-born neurons form the deeper layers, whereas later-born neurons migrate past the existing layers and form the more superficial layers. Reelin, a glycoprotein secreted by Cajal–Retzius neurons in the marginal zone (MZ), is crucial for this “inside-out” layering, because the layers are inverted in the Reelin-deficient mouse, reeler ( Reln rl ). Even though more than a decade has passed since the discovery of reelin , the biological effect of Reelin on individual migrating neurons remains unclear. In addition, although the MZ is missing in the reeler cortex, it is unknown whether Reelin directly regulates the development of the cell-body-sparse MZ. To address these issues, we expressed Reelin ectopically in the developing mouse cortex, and the results showed that Reelin caused the leading processes of migrating neurons to assemble in the Reelin-rich region, which in turn induced their cell bodies to form cellular aggregates around Reelin. Interestingly, the ectopic Reelin-rich region became cell-body-sparse and dendrite-rich, resembling the MZ, and the late-born neurons migrated past their predecessors toward the central Reelin-rich region within the aggregates, resulting in a birthdate-dependent “inside-out” alignment even ectopically. Reelin receptors and intracellular adaptor protein Dab1 were found to be necessary for formation of the aggregates. The above findings indicate that Reelin signaling is capable of inducing the formation of the dendrite-rich, cell-body-sparse MZ and a birthdate-dependent “inside-out” alignment of neurons independently of other factors/structures near the MZ.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2010
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 14 ( 2019-04-02), p. 6914-6923
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 14 ( 2019-04-02), p. 6914-6923
    Abstract: The division of life into producers and consumers is blurred by evolution. For example, eukaryotic phototrophs can lose the capacity to photosynthesize, although they may retain vestigial plastids that perform other essential cellular functions. Chrysophyte algae have undergone a particularly large number of photosynthesis losses. Here, we present a plastid genome sequence from a nonphotosynthetic chrysophyte, “ Spumella ” sp. NIES-1846, and show that it has retained a nearly identical set of plastid-encoded functions as apicomplexan parasites. Our transcriptomic analysis of 12 different photosynthetic and nonphotosynthetic chrysophyte lineages reveals remarkable convergence in the functions of these nonphotosynthetic plastids, along with informative lineage-specific retentions and losses. At one extreme, Cornospumella fuschlensis retains many photosynthesis-associated proteins, although it appears to have lost the reductive pentose phosphate pathway and most plastid amino acid metabolism pathways. At the other extreme, Paraphysomonas lacks plastid-targeted proteins associated with gene expression and all metabolic pathways that require plastid-encoded partners, indicating a complete loss of plastid DNA in this genus. Intriguingly, some of the nucleus-encoded proteins that once functioned in the expression of the Paraphysomonas plastid genome have been retained. These proteins were likely to have been dual targeted to the plastid and mitochondria of the chrysophyte ancestor, and are uniquely targeted to the mitochondria in Paraphysomonas . Our comparative analyses provide insights into the process of functional reduction in nonphotosynthetic plastids.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Association for the Advancement of Science (AAAS) ; 1990
    In:  Science Vol. 247, No. 4940 ( 1990-01-19), p. 324-327
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 247, No. 4940 ( 1990-01-19), p. 324-327
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    RVK:
    RVK:
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 1990
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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