Involvement of Notch Signaling in Hippocampal Synaptic Plasticity
During development of the nervous system, the fate of stem cells is regulated by a cell surface receptor called Notch. Notch is also present in the adult mammalian brain; however, because Notch null mice die during embryonic development, it has proven difficult to determine the functions of Notch. H...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2004-06, Vol.101 (25), p.9458-9462 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Wang, Yue Chan, Sic L. Miele, Lucio Yao, Pamela J. Mackes, Jennifer Ingram, Donald K. Mattson, Mark P. Furukawa, Katsutoshi Andersen, Per O. |
| description | During development of the nervous system, the fate of stem cells is regulated by a cell surface receptor called Notch. Notch is also present in the adult mammalian brain; however, because Notch null mice die during embryonic development, it has proven difficult to determine the functions of Notch. Here, we used Notch antisense transgenic mice that develop and reproduce normally, but exhibit reduced levels of Notch, to demonstrate a role for Notch signaling in synaptic plasticity. Mice with reduced Notch levels exhibit impaired long-term potentiation (LTP) at hippocampal CA1 synapses. A Notch ligand enhances LTP in normal mice and corrects the defect in LTP in Notch antisense transgenic mice. Levels of basal and stimulation-induced NF-κB activity were significantly decreased in mice with reduced Notch levels. These findings suggest an important role for Notch signaling in a form of synaptic plasticity known to be associated with learning and memory processes. |
| doi_str_mv | 10.1073/pnas.0308126101 |
| format | Article |
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Notch is also present in the adult mammalian brain; however, because Notch null mice die during embryonic development, it has proven difficult to determine the functions of Notch. Here, we used Notch antisense transgenic mice that develop and reproduce normally, but exhibit reduced levels of Notch, to demonstrate a role for Notch signaling in synaptic plasticity. Mice with reduced Notch levels exhibit impaired long-term potentiation (LTP) at hippocampal CA1 synapses. A Notch ligand enhances LTP in normal mice and corrects the defect in LTP in Notch antisense transgenic mice. Levels of basal and stimulation-induced NF-κB activity were significantly decreased in mice with reduced Notch levels. These findings suggest an important role for Notch signaling in a form of synaptic plasticity known to be associated with learning and memory processes.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0308126101</identifier><identifier>PMID: 15190179</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Biological Sciences ; Brain research ; Hippocampus ; Hippocampus - physiology ; Learning - physiology ; Ligands ; Long term depression ; Long term potentiation ; Long-Term Potentiation - physiology ; Membrane Proteins - genetics ; Membrane Proteins - physiology ; Memory ; Memory - physiology ; Mice ; Mice, Transgenic ; Neurology ; Neuronal Plasticity - physiology ; Neurons ; Neuroscience ; Presenilins ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - physiology ; Receptors, Notch ; Rodents ; Signal transduction ; Synapses ; Synapses - physiology ; Transgenic animals</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2004-06, Vol.101 (25), p.9458-9462</ispartof><rights>Copyright 1993/2004 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jun 22, 2004</rights><rights>Copyright © 2004, The National Academy of Sciences 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-6de133906a2623beab6a8d8d7c770db31572a3dc5975f31a72a6b3864ace83983</citedby><cites>FETCH-LOGICAL-c590t-6de133906a2623beab6a8d8d7c770db31572a3dc5975f31a72a6b3864ace83983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/101/25.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3372672$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3372672$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15190179$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Chan, Sic L.</creatorcontrib><creatorcontrib>Miele, Lucio</creatorcontrib><creatorcontrib>Yao, Pamela J.</creatorcontrib><creatorcontrib>Mackes, Jennifer</creatorcontrib><creatorcontrib>Ingram, Donald K.</creatorcontrib><creatorcontrib>Mattson, Mark P.</creatorcontrib><creatorcontrib>Furukawa, Katsutoshi</creatorcontrib><creatorcontrib>Andersen, Per O.</creatorcontrib><title>Involvement of Notch Signaling in Hippocampal Synaptic Plasticity</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>During development of the nervous system, the fate of stem cells is regulated by a cell surface receptor called Notch. Notch is also present in the adult mammalian brain; however, because Notch null mice die during embryonic development, it has proven difficult to determine the functions of Notch. Here, we used Notch antisense transgenic mice that develop and reproduce normally, but exhibit reduced levels of Notch, to demonstrate a role for Notch signaling in synaptic plasticity. Mice with reduced Notch levels exhibit impaired long-term potentiation (LTP) at hippocampal CA1 synapses. A Notch ligand enhances LTP in normal mice and corrects the defect in LTP in Notch antisense transgenic mice. Levels of basal and stimulation-induced NF-κB activity were significantly decreased in mice with reduced Notch levels. These findings suggest an important role for Notch signaling in a form of synaptic plasticity known to be associated with learning and memory processes.</description><subject>Animals</subject><subject>Biological Sciences</subject><subject>Brain research</subject><subject>Hippocampus</subject><subject>Hippocampus - physiology</subject><subject>Learning - physiology</subject><subject>Ligands</subject><subject>Long term depression</subject><subject>Long term potentiation</subject><subject>Long-Term Potentiation - physiology</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - physiology</subject><subject>Memory</subject><subject>Memory - physiology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Neurology</subject><subject>Neuronal Plasticity - physiology</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Presenilins</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - physiology</subject><subject>Receptors, Notch</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Synapses</subject><subject>Synapses - physiology</subject><subject>Transgenic animals</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1v0zAUAHALgVhXOHNBEHFAXLI924k_DhymCdikCZAGZ8tJnM6VY4fYqeh_P5dWK3CA05Pl33t6Hwi9wHCGgdPz0et4BhQEJgwDfoQWGCQuWSXhMVoAEF6KilQn6DTGNQDIWsBTdIJrLAFzuUAX134T3MYMxqci9MXnkNq74tauvHbWrwrriys7jqHVw6hdcbv1eky2Lb46HXO0afsMPem1i-b5IS7R948fvl1elTdfPl1fXtyUbS0hlawzmFIJTBNGaGN0w7ToRMdbzqFrKK450bTLmNc9xTq_WEMFq3RrBJWCLtH7fd1xbgbTtbnhSTs1TnbQ01YFbdWfP97eqVXYqIoK-Sv_7SF_Cj9mE5MabGyNc9qbMEfFGKtAiPq_MO9NMiZkhm_-guswT3lxURHAlAPLEy_R-R61U4hxMv1DxxjU7oZqd0N1vGHOePX7oEd_OFoG7w5gl3kshxWplaxqofrZuWR-pkxf_5tm8XIv1jGF6YFQygnjhN4DwLm5cQ</recordid><startdate>20040622</startdate><enddate>20040622</enddate><creator>Wang, Yue</creator><creator>Chan, Sic L.</creator><creator>Miele, Lucio</creator><creator>Yao, Pamela J.</creator><creator>Mackes, Jennifer</creator><creator>Ingram, Donald K.</creator><creator>Mattson, Mark P.</creator><creator>Furukawa, Katsutoshi</creator><creator>Andersen, Per O.</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040622</creationdate><title>Involvement of Notch Signaling in Hippocampal Synaptic Plasticity</title><author>Wang, Yue ; Chan, Sic L. ; Miele, Lucio ; Yao, Pamela J. ; Mackes, Jennifer ; Ingram, Donald K. ; Mattson, Mark P. ; Furukawa, Katsutoshi ; Andersen, Per O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-6de133906a2623beab6a8d8d7c770db31572a3dc5975f31a72a6b3864ace83983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological Sciences</topic><topic>Brain research</topic><topic>Hippocampus</topic><topic>Hippocampus - physiology</topic><topic>Learning - physiology</topic><topic>Ligands</topic><topic>Long term depression</topic><topic>Long term potentiation</topic><topic>Long-Term Potentiation - physiology</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - physiology</topic><topic>Memory</topic><topic>Memory - physiology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Neurology</topic><topic>Neuronal Plasticity - physiology</topic><topic>Neurons</topic><topic>Neuroscience</topic><topic>Presenilins</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - physiology</topic><topic>Receptors, Notch</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Synapses</topic><topic>Synapses - physiology</topic><topic>Transgenic animals</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Chan, Sic L.</creatorcontrib><creatorcontrib>Miele, Lucio</creatorcontrib><creatorcontrib>Yao, Pamela J.</creatorcontrib><creatorcontrib>Mackes, Jennifer</creatorcontrib><creatorcontrib>Ingram, Donald K.</creatorcontrib><creatorcontrib>Mattson, Mark P.</creatorcontrib><creatorcontrib>Furukawa, Katsutoshi</creatorcontrib><creatorcontrib>Andersen, Per O.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yue</au><au>Chan, Sic L.</au><au>Miele, Lucio</au><au>Yao, Pamela J.</au><au>Mackes, Jennifer</au><au>Ingram, Donald K.</au><au>Mattson, Mark P.</au><au>Furukawa, Katsutoshi</au><au>Andersen, Per O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of Notch Signaling in Hippocampal Synaptic Plasticity</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2004-06-22</date><risdate>2004</risdate><volume>101</volume><issue>25</issue><spage>9458</spage><epage>9462</epage><pages>9458-9462</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>During development of the nervous system, the fate of stem cells is regulated by a cell surface receptor called Notch. 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| source | MEDLINE; JSTOR Archive Collection A-Z Listing; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Animals Biological Sciences Brain research Hippocampus Hippocampus - physiology Learning - physiology Ligands Long term depression Long term potentiation Long-Term Potentiation - physiology Membrane Proteins - genetics Membrane Proteins - physiology Memory Memory - physiology Mice Mice, Transgenic Neurology Neuronal Plasticity - physiology Neurons Neuroscience Presenilins Receptors, Cell Surface - genetics Receptors, Cell Surface - physiology Receptors, Notch Rodents Signal transduction Synapses Synapses - physiology Transgenic animals |
| title | Involvement of Notch Signaling in Hippocampal Synaptic Plasticity |
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