Source:http://linkedlifedata.com/resource/pubmed/id/21129439
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2011-1-10
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pubmed:abstractText |
We have reported that systemic application of nicotinic agonists expresses a long-term potentiation (LTP)-like facilitation, a model of synaptic plasticity, in vivo in the mouse hippocampus. The present study conducted to clarify the involvement of synaptotagmin1 in synaptic plasticity by investigating the time-dependent change of the mRNA and protein levels of synaptotagmin1 during LTP-like facilitation in the mouse hippocampus. The mRNA expression of synaptotagmin1 increased during 2- to 8-h period by intraperitoneal application of nicotine (3mg/kg), returning to the basal level in 12-h. Also, the protein level of synaptotagmin1, but not synaptophysin, in a total fraction from hippocampus increased during 4- to 12-h period by the same treatment, returning to the basal level in 24-h. The protein level of synaptotagmin1 in a membrane fraction from hippocampus also increased during 4- to 8-h period by nicotine, returning to the basal level in 12-h. This nicotine-enhanced synaptotagmin1 protein in a membrane fraction was inhibited by pretreatment of mecamylamine (0.3mg/kg, i.p.), a nonselective nicotinic acetylcholine receptors (nAChRs) antagonist. Furthermore, choline (30mg/kg, i.p.), a selective ?7 nAChR agonist, or ABT-418 (10mg/kg, i.p.), a selective ?4?2 nAChR agonist, enhanced the level of synaptotagmin1 in a membrane fraction. Our findings demonstrate that synaptotagmin1 protein following mRNA which is enhanced without increasing the number of synapse gathers around pre-synaptic membrane during hippocampal LTP-like facilitation through activation of ?7 and/or ?4?2 nAChRs in the brain. These results suggest that new-synthesized synaptotagmin1 following synaptic plasticity may contribute to long-lasting synaptic plasticity via positive, feedfoward mechanisms.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1872-7972
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
489
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-9
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pubmed:meshHeading |
pubmed-meshheading:21129439-Animals,
pubmed-meshheading:21129439-Blotting, Western,
pubmed-meshheading:21129439-Gene Expression Regulation,
pubmed-meshheading:21129439-Hippocampus,
pubmed-meshheading:21129439-Long-Term Potentiation,
pubmed-meshheading:21129439-Male,
pubmed-meshheading:21129439-Mice,
pubmed-meshheading:21129439-Mice, Inbred C57BL,
pubmed-meshheading:21129439-RNA, Messenger,
pubmed-meshheading:21129439-Receptors, Nicotinic,
pubmed-meshheading:21129439-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21129439-Synaptotagmin I
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pubmed:year |
2011
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pubmed:articleTitle |
Synaptotagmin1 synthesis induced by synaptic plasticity in mouse hippocampus through activation of nicotinic acetylcholine receptors.
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pubmed:affiliation |
Department of Pharmaceutical Health Care, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, 7-2-1 Kamiohno, Himeji 670-8524, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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