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Soluble Aβ1–42 increases the heterogeneity in synaptic vesicle pool size among synapses by suppressing intersynaptic vesicle sharing
DC Field | Value | Language |
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dc.contributor.author | Park, Daehun | - |
dc.contributor.author | Chang, Sunghoe | - |
dc.date.accessioned | 2018-03-19T00:29:28Z | - |
dc.date.available | 2018-03-19T09:31:31Z | - |
dc.date.issued | 2018-02-20 | - |
dc.identifier.citation | Molecular Brain, 11(1):10 | ko_KR |
dc.identifier.issn | 1756-6606 | - |
dc.identifier.uri | https://hdl.handle.net/10371/139618 | - |
dc.description.abstract | Abstract
Growing evidence has indicated that prefibrillar form of soluble amyloid beta (sAβ1–42) is the major causative factor in the synaptic dysfunction associated with AD. The molecular changes leading to presynaptic dysfunction caused by sAβ1–42, however, still remains elusive. Recently, we found that sAβ1–42 inhibits chemically induced long-term potentiation-induced synaptogenesis by suppressing the intersynaptic vesicle trafficking through calcium (Ca2+) dependent hyperphosphorylation of synapsin and CaMKIV. However, it is still unclear how sAβ1–42 increases intracellular Ca2+ that induces hyperphosphorylation of CaMKIV and synapsin, and what is the functional consequences of sAβ1–42-induced defects in intersynaptic vesicle trafficking in physiological conditions. In this study, we showed that sAβ1–42elevated intracellular Ca2+ through not only extracellular Ca2+ influx but also Ca2+ release from mitochondria. Surprisingly, without Ca2+ release from mitochondria, sAβ1–42 failed to increase intracellular Ca2+ even in the presence of normal extracellular Ca2+. We further found that sAβ1–42-induced mitochondria Ca2+ release alone sufficiently increased Serine 9 phosphorylation of synapsin. By blocking synaptic vesicle reallocation, sAβ1–42 significantly increased heterogeneity of total synaptic vesicle pool size among synapses. Together, our results suggested that by disrupting the axonal vesicle trafficking, sAβ1–42 disabled neurons to adjust synaptic pool sizes among synapses, which might prevent homeostatic rescaling in synaptic strength of individual neurons. | ko_KR |
dc.description.sponsorship | This research was supported by grants from the Brain Research Program (NRF-2017M3C7A1044957–8 and 2015M3C7A1028790) to SC through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning, Republic of Korea. This work was also supported by the Education and Research Encouragement Fund of Seoul National University Hospital. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BioMed Central | ko_KR |
dc.title | Soluble Aβ1–42 increases the heterogeneity in synaptic vesicle pool size among synapses by suppressing intersynaptic vesicle sharing | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 박대훈 | - |
dc.contributor.AlternativeAuthor | 장성호 | - |
dc.identifier.doi | 10.1186/s13041-018-0353-z | - |
dc.rights.holder | The Author(s). | - |
dc.date.updated | 2018-02-25T04:18:22Z | - |
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