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Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system
Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin...
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Lenguaje: | English |
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The Rockefeller University Press
1995
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2120677/ https://www.ncbi.nlm.nih.gov/pubmed/8557745 |
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collection | PubMed |
description | Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure. |
format | Text |
id | pubmed-2120677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1995 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21206772008-05-01 Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system J Cell Biol Articles Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure. The Rockefeller University Press 1995-12-02 /pmc/articles/PMC2120677/ /pubmed/8557745 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title | Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title_full | Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title_fullStr | Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title_full_unstemmed | Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title_short | Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
title_sort | synapsin i deficiency results in the structural change in the presynaptic terminals in the murine nervous system |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2120677/ https://www.ncbi.nlm.nih.gov/pubmed/8557745 |