PSD-95 is required for activity-driven synapse stabilization
The activity-dependent regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and the stabilization of synapses are critical to synaptic development and plasticity. One candidate molecule implicated in maturation, synaptic strengthening, and plasticity is...
Gespeichert in:
| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2007-03, Vol.104 (10), p.4176-4181 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 4181 |
|---|---|
| container_issue | 10 |
| container_start_page | 4176 |
| container_title | Proceedings of the National Academy of Sciences - PNAS |
| container_volume | 104 |
| creator | Ehrlich, Ingrid Klein, Matthew Rumpel, Simon Malinow, Roberto |
| description | The activity-dependent regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and the stabilization of synapses are critical to synaptic development and plasticity. One candidate molecule implicated in maturation, synaptic strengthening, and plasticity is PSD-95. Here we find that acute knockdown of PSD-95 in brain slice cultures by RNAi arrests the normal development of synaptic structure and function that is driven by spontaneous activity. Surprisingly, PSD-95 is not necessary for the induction and early expression of long-term potentiation (LTP). However, knockdown of PSD-95 leads to smaller increases in spine size after chemically induced LTP. Furthermore, although at this age spine turnover is normally low and LTP produces a transient increase, in cells with reduced PSD-95 spine turnover is high and remains increased after LTP. Taken together, our data support a model in which appropriate levels of PSD-95 are required for activity-dependent synapse stabilization after initial phases of synaptic potentiation. |
| doi_str_mv | 10.1073/pnas.0609307104 |
| format | Article |
| fullrecord | <record><control><sourceid>jstor_pubme</sourceid><recordid>TN_cdi_pubmed_primary_17360496</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>25426801</jstor_id><sourcerecordid>25426801</sourcerecordid><originalsourceid>FETCH-LOGICAL-c618t-c5e93e94714f9d04a0a912412b830cb64160acc373d5eb8a15c0cb1b9804a9a93</originalsourceid><addsrcrecordid>eNqFkc9rFDEUx4Modq2ePalDD-Jl2veSTDKBIpT6EwoKteeQyWRqltnJNsksrn-9M-zSVQ96epB83ufl5UvIc4RTBMnO1oNJpyBAMZAI_AFZICgsBVfwkCwAqCxrTvkReZLSEgBUVcNjcoSSCeBKLMj51-t3paoKn4ro7kYfXVt0IRbGZr_xeVu20W_cUKTtYNbJFSmbxvf-p8k-DE_Jo870yT3b12Ny8-H9t8tP5dWXj58vL65KK7DOpa2cYk5xibxTLXADRiHlSJuagW0ERwHGWiZZW7mmNljZ6RgbVU-sMoodk7c773psVq61bsjR9Hod_crErQ7G6z9vBv9d34aNxpqCpPUkeL0XxHA3upT1yifr-t4MLoxJS6CCC0X_C6ISWEmGE3jyF7gMYxymX9AUkDHkch57toNsDClF190_GUHP-ek5P33Ib-p4-fumB34f2AS82gNz50HHZyVHORNv_k3obuz77H7kCX2xQ5cph3jP0opTUQMehnUmaHMbfdI31_N6ALKqpsJ-AZN9wF0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>201331478</pqid></control><display><type>article</type><title>PSD-95 is required for activity-driven synapse stabilization</title><source>MEDLINE</source><source>Jstor Complete Legacy</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Ehrlich, Ingrid ; Klein, Matthew ; Rumpel, Simon ; Malinow, Roberto</creator><creatorcontrib>Ehrlich, Ingrid ; Klein, Matthew ; Rumpel, Simon ; Malinow, Roberto</creatorcontrib><description>The activity-dependent regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and the stabilization of synapses are critical to synaptic development and plasticity. One candidate molecule implicated in maturation, synaptic strengthening, and plasticity is PSD-95. Here we find that acute knockdown of PSD-95 in brain slice cultures by RNAi arrests the normal development of synaptic structure and function that is driven by spontaneous activity. Surprisingly, PSD-95 is not necessary for the induction and early expression of long-term potentiation (LTP). However, knockdown of PSD-95 leads to smaller increases in spine size after chemically induced LTP. Furthermore, although at this age spine turnover is normally low and LTP produces a transient increase, in cells with reduced PSD-95 spine turnover is high and remains increased after LTP. Taken together, our data support a model in which appropriate levels of PSD-95 are required for activity-dependent synapse stabilization after initial phases of synaptic potentiation.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0609307104</identifier><identifier>PMID: 17360496</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Biological Sciences ; Brain ; Brain - metabolism ; Cells ; Dendrites ; Dendrites - metabolism ; Disks Large Homolog 4 Protein ; Electrophysiology ; Glutamine - metabolism ; Hippocampus - metabolism ; Image Processing, Computer-Assisted ; Intracellular Signaling Peptides and Proteins - metabolism ; Intracellular Signaling Peptides and Proteins - physiology ; Long term depression ; Long term potentiation ; Membrane Proteins - metabolism ; Membrane Proteins - physiology ; Micrometers ; Mushrooms ; Neuronal Plasticity ; Neurons ; Neuroscience ; Neurosciences ; Proteins ; Rats ; Receptors ; Receptors, AMPA - metabolism ; RNA Interference ; Synapses ; Synapses - metabolism ; Synapses - pathology ; Synaptic Transmission</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2007-03, Vol.104 (10), p.4176-4181</ispartof><rights>Copyright 2007 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Mar 6, 2007</rights><rights>2007 by The National Academy of Sciences of the USA 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c618t-c5e93e94714f9d04a0a912412b830cb64160acc373d5eb8a15c0cb1b9804a9a93</citedby><cites>FETCH-LOGICAL-c618t-c5e93e94714f9d04a0a912412b830cb64160acc373d5eb8a15c0cb1b9804a9a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/104/10.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25426801$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25426801$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27903,27904,53769,53771,57995,58228</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17360496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ehrlich, Ingrid</creatorcontrib><creatorcontrib>Klein, Matthew</creatorcontrib><creatorcontrib>Rumpel, Simon</creatorcontrib><creatorcontrib>Malinow, Roberto</creatorcontrib><title>PSD-95 is required for activity-driven synapse stabilization</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The activity-dependent regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and the stabilization of synapses are critical to synaptic development and plasticity. One candidate molecule implicated in maturation, synaptic strengthening, and plasticity is PSD-95. Here we find that acute knockdown of PSD-95 in brain slice cultures by RNAi arrests the normal development of synaptic structure and function that is driven by spontaneous activity. Surprisingly, PSD-95 is not necessary for the induction and early expression of long-term potentiation (LTP). However, knockdown of PSD-95 leads to smaller increases in spine size after chemically induced LTP. Furthermore, although at this age spine turnover is normally low and LTP produces a transient increase, in cells with reduced PSD-95 spine turnover is high and remains increased after LTP. Taken together, our data support a model in which appropriate levels of PSD-95 are required for activity-dependent synapse stabilization after initial phases of synaptic potentiation.</description><subject>Animals</subject><subject>Biological Sciences</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Cells</subject><subject>Dendrites</subject><subject>Dendrites - metabolism</subject><subject>Disks Large Homolog 4 Protein</subject><subject>Electrophysiology</subject><subject>Glutamine - metabolism</subject><subject>Hippocampus - metabolism</subject><subject>Image Processing, Computer-Assisted</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins - physiology</subject><subject>Long term depression</subject><subject>Long term potentiation</subject><subject>Membrane Proteins - metabolism</subject><subject>Membrane Proteins - physiology</subject><subject>Micrometers</subject><subject>Mushrooms</subject><subject>Neuronal Plasticity</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Neurosciences</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptors</subject><subject>Receptors, AMPA - metabolism</subject><subject>RNA Interference</subject><subject>Synapses</subject><subject>Synapses - metabolism</subject><subject>Synapses - pathology</subject><subject>Synaptic Transmission</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9rFDEUx4Modq2ePalDD-Jl2veSTDKBIpT6EwoKteeQyWRqltnJNsksrn-9M-zSVQ96epB83ufl5UvIc4RTBMnO1oNJpyBAMZAI_AFZICgsBVfwkCwAqCxrTvkReZLSEgBUVcNjcoSSCeBKLMj51-t3paoKn4ro7kYfXVt0IRbGZr_xeVu20W_cUKTtYNbJFSmbxvf-p8k-DE_Jo870yT3b12Ny8-H9t8tP5dWXj58vL65KK7DOpa2cYk5xibxTLXADRiHlSJuagW0ERwHGWiZZW7mmNljZ6RgbVU-sMoodk7c773psVq61bsjR9Hod_crErQ7G6z9vBv9d34aNxpqCpPUkeL0XxHA3upT1yifr-t4MLoxJS6CCC0X_C6ISWEmGE3jyF7gMYxymX9AUkDHkch57toNsDClF190_GUHP-ek5P33Ib-p4-fumB34f2AS82gNz50HHZyVHORNv_k3obuz77H7kCX2xQ5cph3jP0opTUQMehnUmaHMbfdI31_N6ALKqpsJ-AZN9wF0</recordid><startdate>20070306</startdate><enddate>20070306</enddate><creator>Ehrlich, Ingrid</creator><creator>Klein, Matthew</creator><creator>Rumpel, Simon</creator><creator>Malinow, Roberto</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</scope><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>20070306</creationdate><title>PSD-95 is required for activity-driven synapse stabilization</title><author>Ehrlich, Ingrid ; Klein, Matthew ; Rumpel, Simon ; Malinow, Roberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c618t-c5e93e94714f9d04a0a912412b830cb64160acc373d5eb8a15c0cb1b9804a9a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological Sciences</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Cells</topic><topic>Dendrites</topic><topic>Dendrites - metabolism</topic><topic>Disks Large Homolog 4 Protein</topic><topic>Electrophysiology</topic><topic>Glutamine - metabolism</topic><topic>Hippocampus - metabolism</topic><topic>Image Processing, Computer-Assisted</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Intracellular Signaling Peptides and Proteins - physiology</topic><topic>Long term depression</topic><topic>Long term potentiation</topic><topic>Membrane Proteins - metabolism</topic><topic>Membrane Proteins - physiology</topic><topic>Micrometers</topic><topic>Mushrooms</topic><topic>Neuronal Plasticity</topic><topic>Neurons</topic><topic>Neuroscience</topic><topic>Neurosciences</topic><topic>Proteins</topic><topic>Rats</topic><topic>Receptors</topic><topic>Receptors, AMPA - metabolism</topic><topic>RNA Interference</topic><topic>Synapses</topic><topic>Synapses - metabolism</topic><topic>Synapses - pathology</topic><topic>Synaptic Transmission</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ehrlich, Ingrid</creatorcontrib><creatorcontrib>Klein, Matthew</creatorcontrib><creatorcontrib>Rumpel, Simon</creatorcontrib><creatorcontrib>Malinow, Roberto</creatorcontrib><collection>AGRIS</collection><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>Ehrlich, Ingrid</au><au>Klein, Matthew</au><au>Rumpel, Simon</au><au>Malinow, Roberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PSD-95 is required for activity-driven synapse stabilization</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2007-03-06</date><risdate>2007</risdate><volume>104</volume><issue>10</issue><spage>4176</spage><epage>4181</epage><pages>4176-4181</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>The activity-dependent regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and the stabilization of synapses are critical to synaptic development and plasticity. One candidate molecule implicated in maturation, synaptic strengthening, and plasticity is PSD-95. Here we find that acute knockdown of PSD-95 in brain slice cultures by RNAi arrests the normal development of synaptic structure and function that is driven by spontaneous activity. Surprisingly, PSD-95 is not necessary for the induction and early expression of long-term potentiation (LTP). However, knockdown of PSD-95 leads to smaller increases in spine size after chemically induced LTP. Furthermore, although at this age spine turnover is normally low and LTP produces a transient increase, in cells with reduced PSD-95 spine turnover is high and remains increased after LTP. Taken together, our data support a model in which appropriate levels of PSD-95 are required for activity-dependent synapse stabilization after initial phases of synaptic potentiation.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>17360496</pmid><doi>10.1073/pnas.0609307104</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0027-8424 |
| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2007-03, Vol.104 (10), p.4176-4181 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_pubmed_primary_17360496 |
| source | MEDLINE; Jstor Complete Legacy; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Animals Biological Sciences Brain Brain - metabolism Cells Dendrites Dendrites - metabolism Disks Large Homolog 4 Protein Electrophysiology Glutamine - metabolism Hippocampus - metabolism Image Processing, Computer-Assisted Intracellular Signaling Peptides and Proteins - metabolism Intracellular Signaling Peptides and Proteins - physiology Long term depression Long term potentiation Membrane Proteins - metabolism Membrane Proteins - physiology Micrometers Mushrooms Neuronal Plasticity Neurons Neuroscience Neurosciences Proteins Rats Receptors Receptors, AMPA - metabolism RNA Interference Synapses Synapses - metabolism Synapses - pathology Synaptic Transmission |
| title | PSD-95 is required for activity-driven synapse stabilization |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-25T23%3A54%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PSD-95%20is%20required%20for%20activity-driven%20synapse%20stabilization&rft.jtitle=Proceedings%20of%20the%20National%20Academy%20of%20Sciences%20-%20PNAS&rft.au=Ehrlich,%20Ingrid&rft.date=2007-03-06&rft.volume=104&rft.issue=10&rft.spage=4176&rft.epage=4181&rft.pages=4176-4181&rft.issn=0027-8424&rft.eissn=1091-6490&rft_id=info:doi/10.1073/pnas.0609307104&rft_dat=%3Cjstor_pubme%3E25426801%3C/jstor_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=201331478&rft_id=info:pmid/17360496&rft_jstor_id=25426801&rfr_iscdi=true |