Abstract：
:Short-term synaptic plasticity is a defining feature of neuronal activity, but the underlying molecular mechanisms are poorly understood. Depression of synaptic activity might be due to limited vesicle availability, whereas facilitation is thought to result from elevated calcium levels. However, it is unclear whether the strength and direction (facilitation versus depression) of plasticity at a given synapse result from preexisting synaptic strength or whether they are regulated by separate mechanisms. Here we show, in rat hippocampal cell cultures, that increases in the calcium binding protein neuronal calcium sensor-1 (NCS-1) can switch paired-pulse depression to facilitation without altering basal synaptic transmission or initial neurotransmitter release probability. Facilitation persisted during high-frequency trains of stimulation, indicating that NCS-1 can recruit 'dormant' vesicles. Our results suggest that NCS-1 acts as a calcium sensor for short-term plasticity by facilitating neurotransmitter output independent of initial release. We conclude that separate mechanisms are responsible for determining basal synaptic strength and short-term plasticity.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Sippy T,Cruz-Martín A,Jeromin A,Schweizer FEdoi
10.1038/nn1117subject
Has Abstractpub_date
2003-10-01 00:00:00pages
1031-8issue
10eissn
1097-6256issn
1546-1726pii
nn1117journal_volume
6pub_type
杂志文章abstract：:Independent evidence associates β-amyloid pathology with both non-rapid eye movement (NREM) sleep disruption and memory impairment in older adults. However, whether the influence of β-amyloid pathology on hippocampus-dependent memory is, in part, driven by impairments of NREM slow wave activity (SWA) and associated ov...
journal_title：Nature neuroscience
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更新日期：2015-07-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
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更新日期：2016-09-27 00:00:00
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pub_type： 杂志文章
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更新日期：2015-05-01 00:00:00
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更新日期：2008-02-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/nn.4133
更新日期：2015-11-01 00:00:00
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journal_title：Nature neuroscience
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更新日期：2014-08-01 00:00:00
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更新日期：2018-05-01 00:00:00
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pub_type： 已发布勘误
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更新日期：2018-09-01 00:00:00
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pub_type： 杂志文章
doi：10.1038/nn.3397
更新日期：2013-06-01 00:00:00
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doi：10.1038/s41593-018-0144-y
更新日期：2018-06-01 00:00:00
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pub_type： 杂志文章
doi：10.1038/nn1256
更新日期：2004-06-01 00:00:00
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更新日期：2002-11-01 00:00:00
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pub_type： 杂志文章
doi：10.1038/nn.3862
更新日期：2014-12-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章,评审
doi：10.1038/nn.2647
更新日期：2010-10-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/nn.3505
更新日期：2013-10-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/nn.4444
更新日期：2017-01-01 00:00:00
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pub_type： 杂志文章
doi：10.1038/10217
更新日期：1999-07-01 00:00:00
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更新日期：2006-03-01 00:00:00
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doi：10.1038/nn.3592
更新日期：2014-01-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/nn.2841
更新日期：2011-06-26 00:00:00
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更新日期：2004-04-01 00:00:00
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journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/80577
更新日期：2000-11-01 00:00:00
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更新日期：2011-09-27 00:00:00
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journal_title：Nature neuroscience
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doi：10.1038/nn1904
更新日期：2007-06-01 00:00:00
abstract：:The morphological transition of growth cones to synaptic boutons characterizes synaptogenesis. Here we have isolated mutations in immaculate connections (imac; CG8566), a previously uncharacterized Drosophila gene encoding a member of the Kinesin-3 family. Whereas earlier studies in Drosophila implicated Kinesin-1 in ...
journal_title：Nature neuroscience
pub_type： 杂志文章
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更新日期：2007-08-01 00:00:00
abstract：:Neuregulin 1 type III is processed following regulated intramembrane proteolysis, which allows communication from the plasma membrane to the nucleus. We found that the intracellular domain of neuregulin 1 type III upregulated the prostaglandin D2 synthase (L-pgds, also known as Ptgds) gene, which, together with the G ...
journal_title：Nature neuroscience
pub_type： 杂志文章
doi：10.1038/nn.3857
更新日期：2014-12-01 00:00:00
