Source:http://linkedlifedata.com/resource/pubmed/id/12896973
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
42
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| pubmed:dateCreated |
2003-10-13
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| pubmed:abstractText |
Voltage-gated calcium channels couple changes in membrane potential to neuronal functions regulated by calcium, including neurotransmitter release. Here we report that presynaptic N-type calcium channels not only control neurotransmitter release but also regulate synaptic growth at Drosophila neuromuscular junctions. In a screen for behavioral mutants that disrupt synaptic transmission, an allele of the N-type calcium channel locus (Dmca1A) was identified that caused synaptic undergrowth. The underlying molecular defect was identified as a neutralization of a charged residue in the third S4 voltage sensor. RNA interference reduction of N-type calcium channel expression also reduced synaptic growth. Hypomorphic mutations in syntaxin-1A or n-synaptobrevin, which also disrupt neurotransmitter release, did not affect synapse proliferation at the neuromuscular junction, suggesting calcium entry through presynaptic N-type calcium channels, not neurotransmitter release per se, is important for synaptic growth. The reduced synapse proliferation in Dmca1A mutants is not due to increased synapse retraction but instead reflects a role for calcium influx in synaptic growth mechanisms. These results suggest N-type channels participate in synaptic growth through signaling pathways that are distinct from those that mediate neurotransmitter release. Linking presynaptic voltage-gated calcium entry to downstream calcium-sensitive synaptic growth regulators provides an efficient activity-dependent mechanism for modifying synaptic strength.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, N-Type,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Double-Stranded,
http://linkedlifedata.com/resource/pubmed/chemical/cac protein, Drosophila
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0021-9258
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
17
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| pubmed:volume |
278
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
41099-108
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| pubmed:dateRevised |
2011-3-2
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| pubmed:meshHeading |
pubmed-meshheading:12896973-Alleles,
pubmed-meshheading:12896973-Amino Acid Sequence,
pubmed-meshheading:12896973-Animals,
pubmed-meshheading:12896973-Calcium,
pubmed-meshheading:12896973-Calcium Channels,
pubmed-meshheading:12896973-Calcium Channels, N-Type,
pubmed-meshheading:12896973-DNA,
pubmed-meshheading:12896973-Dose-Response Relationship, Drug,
pubmed-meshheading:12896973-Drosophila,
pubmed-meshheading:12896973-Drosophila Proteins,
pubmed-meshheading:12896973-Electrophysiology,
pubmed-meshheading:12896973-Immunohistochemistry,
pubmed-meshheading:12896973-Microscopy, Fluorescence,
pubmed-meshheading:12896973-Models, Biological,
pubmed-meshheading:12896973-Molecular Sequence Data,
pubmed-meshheading:12896973-Mutation,
pubmed-meshheading:12896973-Phylogeny,
pubmed-meshheading:12896973-RNA, Double-Stranded,
pubmed-meshheading:12896973-RNA Interference,
pubmed-meshheading:12896973-Synapses,
pubmed-meshheading:12896973-Temperature,
pubmed-meshheading:12896973-Time Factors
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| pubmed:year |
2003
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| pubmed:articleTitle |
Presynaptic N-type calcium channels regulate synaptic growth.
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| pubmed:affiliation |
Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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