Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons
Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in...
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creator | Oettinghaus, B Schulz, J M Restelli, L M Licci, M Savoia, C Schmidt, A Schmitt, K Grimm, A Morè, L Hench, J Tolnay, M Eckert, A D'Adamo, P Franken, P Ishihara, N Mihara, K Bischofberger, J Scorrano, L Frank, S |
description | Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in adult neurons remains unclear. Here we show that inducible
Drp1
ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic
Drp1
ablation. Collectively, our
in vivo
observations clarify the role of mitochondrial fission in neurons, demonstrating that
Drp1
ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration. |
doi_str_mv | 10.1038/cdd.2015.39 |
format | Article |
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Drp1
ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic
Drp1
ablation. Collectively, our
in vivo
observations clarify the role of mitochondrial fission in neurons, demonstrating that
Drp1
ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2015.39</identifier><identifier>PMID: 25909888</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/378 ; Animals ; Antioxidants - administration & dosage ; Apoptosis ; Atrophy - genetics ; Atrophy - metabolism ; Atrophy - pathology ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Cycle Analysis ; Dynamins - biosynthesis ; Dynamins - genetics ; Hippocampus - growth & development ; Hippocampus - metabolism ; Hippocampus - pathology ; Life Sciences ; Memory Disorders - genetics ; Memory Disorders - pathology ; Mice ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial Dynamics - genetics ; Nerve Degeneration - genetics ; Nerve Degeneration - metabolism ; Nerve Degeneration - pathology ; Nervous System - growth & development ; Nervous System - pathology ; Neurons - metabolism ; Neurons - pathology ; Original Paper ; Prosencephalon - growth & development ; Prosencephalon - metabolism ; Prosencephalon - pathology ; Stem Cells</subject><ispartof>Cell death and differentiation, 2016-01, Vol.23 (1), p.18-28</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Jan 2016</rights><rights>Copyright © 2016 Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c615t-f26fe8529d78ae3ab62ff5c34f1add23b19927d608dcb0b196d14525796a6aaa3</citedby><cites>FETCH-LOGICAL-c615t-f26fe8529d78ae3ab62ff5c34f1add23b19927d608dcb0b196d14525796a6aaa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815974/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815974/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25909888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oettinghaus, B</creatorcontrib><creatorcontrib>Schulz, J M</creatorcontrib><creatorcontrib>Restelli, L M</creatorcontrib><creatorcontrib>Licci, M</creatorcontrib><creatorcontrib>Savoia, C</creatorcontrib><creatorcontrib>Schmidt, A</creatorcontrib><creatorcontrib>Schmitt, K</creatorcontrib><creatorcontrib>Grimm, A</creatorcontrib><creatorcontrib>Morè, L</creatorcontrib><creatorcontrib>Hench, J</creatorcontrib><creatorcontrib>Tolnay, M</creatorcontrib><creatorcontrib>Eckert, A</creatorcontrib><creatorcontrib>D'Adamo, P</creatorcontrib><creatorcontrib>Franken, P</creatorcontrib><creatorcontrib>Ishihara, N</creatorcontrib><creatorcontrib>Mihara, K</creatorcontrib><creatorcontrib>Bischofberger, J</creatorcontrib><creatorcontrib>Scorrano, L</creatorcontrib><creatorcontrib>Frank, S</creatorcontrib><title>Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in adult neurons remains unclear. Here we show that inducible
Drp1
ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic
Drp1
ablation. Collectively, our
in vivo
observations clarify the role of mitochondrial fission in neurons, demonstrating that
Drp1
ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration.</description><subject>631/378</subject><subject>Animals</subject><subject>Antioxidants - administration & dosage</subject><subject>Apoptosis</subject><subject>Atrophy - genetics</subject><subject>Atrophy - metabolism</subject><subject>Atrophy - pathology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Dynamins - biosynthesis</subject><subject>Dynamins - genetics</subject><subject>Hippocampus - growth & development</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Life Sciences</subject><subject>Memory Disorders - genetics</subject><subject>Memory Disorders - pathology</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial Dynamics - genetics</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - pathology</subject><subject>Nervous System - growth & development</subject><subject>Nervous System - pathology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Original Paper</subject><subject>Prosencephalon - growth & development</subject><subject>Prosencephalon - metabolism</subject><subject>Prosencephalon - pathology</subject><subject>Stem Cells</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkstrFTEUxgdRbK2u3EvAjWDnmkwek2wKUnxBwYW6Dmfy6E2ZScZkRrhL_3Mz3FqqCK6Sw_fLd3KSr2meE7wjmMo3xtpdhwnfUfWgOSWsFy1nmD6se8pxqzDrT5onpdxgjEWvxOPmpOMKKynlafPzyyHCvASD7KH4NZolpHiOJjelfEDW-WDCUhBEi_ZhnpOBaYYRwZLTvK_A6tCSEAwjbAdR8mgKSzL7FG0OFfShlE0IEYFdxwX5lN2QodbRrTnF8rR55GEs7tntetZ8e__u6-XH9urzh0-Xb69aIwhfWt8J7yTvlO0lOAqD6LznhjJPwNqODkSprrcCS2sGXCthCeMdrwODAAB61lwcfed1mJw1Li4ZRj3nMEE-6ARB_6nEsNfX6YdmknDVs2rw6tYgp--rK4ueQjFuHCG6tBZNJO0pZkyq_6M9E7LHisuKvvwLvUlrjvUlNooJRjpFK_X6SJmcSsnO392bYL2lQNcU6C0Fmm7tX9wf9Y79_e0VOD8CpUrx2uV7Tf_h9wuZBr-p</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Oettinghaus, B</creator><creator>Schulz, J M</creator><creator>Restelli, L M</creator><creator>Licci, M</creator><creator>Savoia, C</creator><creator>Schmidt, A</creator><creator>Schmitt, K</creator><creator>Grimm, A</creator><creator>Morè, L</creator><creator>Hench, J</creator><creator>Tolnay, M</creator><creator>Eckert, A</creator><creator>D'Adamo, P</creator><creator>Franken, P</creator><creator>Ishihara, N</creator><creator>Mihara, K</creator><creator>Bischofberger, J</creator><creator>Scorrano, L</creator><creator>Frank, S</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160101</creationdate><title>Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons</title><author>Oettinghaus, B ; Schulz, J M ; Restelli, L M ; Licci, M ; Savoia, C ; Schmidt, A ; Schmitt, K ; Grimm, A ; Morè, L ; Hench, J ; Tolnay, M ; Eckert, A ; D'Adamo, P ; Franken, P ; Ishihara, N ; Mihara, K ; Bischofberger, J ; Scorrano, L ; Frank, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c615t-f26fe8529d78ae3ab62ff5c34f1add23b19927d608dcb0b196d14525796a6aaa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>631/378</topic><topic>Animals</topic><topic>Antioxidants - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oettinghaus, B</au><au>Schulz, J M</au><au>Restelli, L M</au><au>Licci, M</au><au>Savoia, C</au><au>Schmidt, A</au><au>Schmitt, K</au><au>Grimm, A</au><au>Morè, L</au><au>Hench, J</au><au>Tolnay, M</au><au>Eckert, A</au><au>D'Adamo, P</au><au>Franken, P</au><au>Ishihara, N</au><au>Mihara, K</au><au>Bischofberger, J</au><au>Scorrano, L</au><au>Frank, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>23</volume><issue>1</issue><spage>18</spage><epage>28</epage><pages>18-28</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in adult neurons remains unclear. Here we show that inducible
Drp1
ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic
Drp1
ablation. Collectively, our
in vivo
observations clarify the role of mitochondrial fission in neurons, demonstrating that
Drp1
ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25909888</pmid><doi>10.1038/cdd.2015.39</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/378 Animals Antioxidants - administration & dosage Apoptosis Atrophy - genetics Atrophy - metabolism Atrophy - pathology Biochemistry Biomedical and Life Sciences Cell Biology Cell Cycle Analysis Dynamins - biosynthesis Dynamins - genetics Hippocampus - growth & development Hippocampus - metabolism Hippocampus - pathology Life Sciences Memory Disorders - genetics Memory Disorders - pathology Mice Mitochondria - metabolism Mitochondria - pathology Mitochondrial Dynamics - genetics Nerve Degeneration - genetics Nerve Degeneration - metabolism Nerve Degeneration - pathology Nervous System - growth & development Nervous System - pathology Neurons - metabolism Neurons - pathology Original Paper Prosencephalon - growth & development Prosencephalon - metabolism Prosencephalon - pathology Stem Cells |
title | Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons |
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