Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death
: The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3‐month‐old rats. Sham surgery was performed on age‐matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric d...
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Veröffentlicht in: | Annals of the New York Academy of Sciences 2006-12, Vol.1090 (1), p.26-34 |
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creator | BERTONI-FREDDARI, CARLO FATTORETTI, PATRIZIA CASOLI, TIZIANA DI STEFANO, GIUSEPPINA SOLAZZI, MORENO PERNA, ELISA DE ANGELIS, CLARA |
description | : The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3‐month‐old rats. Sham surgery was performed on age‐matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer‐assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well‐documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke. |
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Sham surgery was performed on age‐matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer‐assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well‐documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>EISSN: 1930-6547</identifier><identifier>DOI: 10.1196/annals.1378.003</identifier><identifier>PMID: 17384244</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Animals ; Brain Ischemia - pathology ; CA1 neurons ; Cell Death ; experimental ischemia-delayed cell death ; Female ; mitochondrial structural dynamics ; morphometry ; Neurons - pathology ; Rats ; Rats, Inbred WKY ; Synapses ; synaptic mitochondria</subject><ispartof>Annals of the New York Academy of Sciences, 2006-12, Vol.1090 (1), p.26-34</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3633-689a18b3ef854596bca7a6d19b4f3b86dea5ddae72bffdece03310c8e0500ae23</citedby><cites>FETCH-LOGICAL-c3633-689a18b3ef854596bca7a6d19b4f3b86dea5ddae72bffdece03310c8e0500ae23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1196%2Fannals.1378.003$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1196%2Fannals.1378.003$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17384244$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BERTONI-FREDDARI, CARLO</creatorcontrib><creatorcontrib>FATTORETTI, PATRIZIA</creatorcontrib><creatorcontrib>CASOLI, TIZIANA</creatorcontrib><creatorcontrib>DI STEFANO, GIUSEPPINA</creatorcontrib><creatorcontrib>SOLAZZI, MORENO</creatorcontrib><creatorcontrib>PERNA, ELISA</creatorcontrib><creatorcontrib>DE ANGELIS, CLARA</creatorcontrib><title>Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>: The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3‐month‐old rats. Sham surgery was performed on age‐matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer‐assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well‐documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke.</description><subject>Animals</subject><subject>Brain Ischemia - pathology</subject><subject>CA1 neurons</subject><subject>Cell Death</subject><subject>experimental ischemia-delayed cell death</subject><subject>Female</subject><subject>mitochondrial structural dynamics</subject><subject>morphometry</subject><subject>Neurons - pathology</subject><subject>Rats</subject><subject>Rats, Inbred WKY</subject><subject>Synapses</subject><subject>synaptic mitochondria</subject><issn>0077-8923</issn><issn>1749-6632</issn><issn>1930-6547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFv0zAUhy0EYmVw5oZ84pbu2S-xnePYoEzaiqBDwMlynBfVkCbFToD-96RKBced_A7f95P1MfZSwFKIUl24rnNtWgrUZgmAj9hC6LzMlEL5mC0AtM5MKfGMPUvpO4CQJtdP2ZnQaHKZ5wv29RM5P4RfxDdDHP0wRtfy60PndsEn3jd8M937IXh-F4beb_uujsHx0PGb5Lc0UfyaWnegmq9pjH131MkN2-fsSTN9jV6c3nP2-d3b-6v32e2H1c3V5W3mUSFmypROmAqpMUVelKryTjtVi7LKG6yMqskVde1Iy6ppavIEiAK8ISgAHEk8Z6_n3X3sf46UBrsLyVPbuo76MVllEEEbeBCUUMpCq2ICL2bQxz6lSI3dx7Bz8WAF2GN1O1e3x-p2qj4Zr07TY7Wj-j9_yjwBcgZ-h5YOD-3Z9bfLzXE1m6WQBvrzT3Lxh1UadWG_rFcW8_s7-PimsCv8C6oLnzs</recordid><startdate>200612</startdate><enddate>200612</enddate><creator>BERTONI-FREDDARI, CARLO</creator><creator>FATTORETTI, PATRIZIA</creator><creator>CASOLI, TIZIANA</creator><creator>DI STEFANO, GIUSEPPINA</creator><creator>SOLAZZI, MORENO</creator><creator>PERNA, ELISA</creator><creator>DE ANGELIS, CLARA</creator><general>Blackwell Publishing Inc</general><scope>BSCLL</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>200612</creationdate><title>Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death</title><author>BERTONI-FREDDARI, CARLO ; FATTORETTI, PATRIZIA ; CASOLI, TIZIANA ; DI STEFANO, GIUSEPPINA ; SOLAZZI, MORENO ; PERNA, ELISA ; DE ANGELIS, CLARA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3633-689a18b3ef854596bca7a6d19b4f3b86dea5ddae72bffdece03310c8e0500ae23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Brain Ischemia - pathology</topic><topic>CA1 neurons</topic><topic>Cell Death</topic><topic>experimental ischemia-delayed cell death</topic><topic>Female</topic><topic>mitochondrial structural dynamics</topic><topic>morphometry</topic><topic>Neurons - pathology</topic><topic>Rats</topic><topic>Rats, Inbred WKY</topic><topic>Synapses</topic><topic>synaptic mitochondria</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BERTONI-FREDDARI, CARLO</creatorcontrib><creatorcontrib>FATTORETTI, PATRIZIA</creatorcontrib><creatorcontrib>CASOLI, TIZIANA</creatorcontrib><creatorcontrib>DI STEFANO, GIUSEPPINA</creatorcontrib><creatorcontrib>SOLAZZI, MORENO</creatorcontrib><creatorcontrib>PERNA, ELISA</creatorcontrib><creatorcontrib>DE ANGELIS, CLARA</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BERTONI-FREDDARI, CARLO</au><au>FATTORETTI, PATRIZIA</au><au>CASOLI, TIZIANA</au><au>DI STEFANO, GIUSEPPINA</au><au>SOLAZZI, MORENO</au><au>PERNA, ELISA</au><au>DE ANGELIS, CLARA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2006-12</date><risdate>2006</risdate><volume>1090</volume><issue>1</issue><spage>26</spage><epage>34</epage><pages>26-34</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><eissn>1930-6547</eissn><abstract>: The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3‐month‐old rats. Sham surgery was performed on age‐matched controls. The number of mitochondria/μm3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer‐assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well‐documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>17384244</pmid><doi>10.1196/annals.1378.003</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Brain Ischemia - pathology CA1 neurons Cell Death experimental ischemia-delayed cell death Female mitochondrial structural dynamics morphometry Neurons - pathology Rats Rats, Inbred WKY Synapses synaptic mitochondria |
title | Reactive Structural Dynamics of Synaptic Mitochondria in Ischemic Delayed Neuronal Death |
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