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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interactions between mitochondria and the transcription factor myocyte enhancer factor 2 (MEF2) regulate neuronal structural and functional plasticity and metaplasticity</title><author><name sortKey="Brusco, Janaina" sort="Brusco, Janaina" uniqKey="Brusco J" first="Janaina" last="Brusco">Janaina Brusco</name></author><author><name sortKey="Haas, Kurt" sort="Haas, Kurt" uniqKey="Haas K" first="Kurt" last="Haas">Kurt Haas</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25581818</idno><idno type="pmc">4560579</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560579</idno><idno type="RBID">PMC:4560579</idno><idno type="doi">10.1113/jphysiol.2014.282459</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000105</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000105</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Interactions between mitochondria and the transcription factor myocyte enhancer factor 2 (MEF2) regulate neuronal structural and functional plasticity and metaplasticity</title><author><name sortKey="Brusco, Janaina" sort="Brusco, Janaina" uniqKey="Brusco J" first="Janaina" last="Brusco">Janaina Brusco</name></author><author><name sortKey="Haas, Kurt" sort="Haas, Kurt" uniqKey="Haas K" first="Kurt" last="Haas">Kurt Haas</name></author></analytic><series><title level="j">The Journal of Physiology</title><idno type="ISSN">0022-3751</idno><idno type="eISSN">1469-7793</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The classical view of mitochondria as housekeeping organelles acting in the background to simply maintain cellular energy demands has been challenged by mounting evidence of their direct and active participation in synaptic plasticity in neurons. Time-lapse imaging has revealed that mitochondria are motile in dendrites, with their localization and fusion and fission events regulated by synaptic activity. The positioning of mitochondria directly influences function of nearby synapses through multiple pathways including control over local concentrations of ATP, Ca<sup>2+</sup> and reactive oxygen species. Recent studies have also shown that mitochondrial protein cascades, classically associated with apoptosis, are involved in neural plasticity in healthy cells. These findings link mitochondria to the plasticity- and metaplasticity-associated activity-dependent transcription factor myocyte enhancer factor 2 (MEF2), further repositioning mitochondria as potential command centres for regulation of synaptic plasticity. Intriguingly, MEF2 and mitochondrial functions appear to be intricately intertwined, as MEF2 is a target of mitochondrial apoptotic caspases and, in turn, MEF2 regulates mitochondrial genome transcription essential for production of superoxidase and hydrogen peroxidase. Here, we review evidence supporting mitochondria as central organelles controlling the spatiotemporal expression of neuronal plasticity, and attempt to disentangle the MEF2–mitochondria relationship mediating these functions.</p></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Physiol</journal-id><journal-id journal-id-type="iso-abbrev">J. Physiol. (Lond.)</journal-id><journal-id journal-id-type="publisher-id">tjp</journal-id><journal-title-group><journal-title>The Journal of Physiology</journal-title></journal-title-group><issn pub-type="ppub">0022-3751</issn><issn pub-type="epub">1469-7793</issn><publisher><publisher-name>John Wiley & Sons, Ltd</publisher-name><publisher-loc>Chichester, UK</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25581818</article-id><article-id pub-id-type="pmc">4560579</article-id><article-id pub-id-type="doi">10.1113/jphysiol.2014.282459</article-id><article-categories><subj-group subj-group-type="heading"><subject>Symposium Section Reviews: Coupling Cellular Metabolism to Neuronal Signalling</subject></subj-group></article-categories><title-group><article-title>Interactions between mitochondria and the transcription factor myocyte enhancer factor 2 (MEF2) regulate neuronal structural and functional plasticity and metaplasticity</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Brusco</surname><given-names>Janaina</given-names></name></contrib><contrib contrib-type="author"><name><surname>Haas</surname><given-names>Kurt</given-names></name></contrib><aff><institution>Department of Cellular and Physiological Sciences and the Brain Research Centre, University of British Columbia</institution><addr-line>Vancouver, BC, Canada, V6T2B5</addr-line></aff></contrib-group><author-notes><corresp id="cor1"><bold>Corresponding author</bold> K. Haas: Brain Research Centre, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T2B5. Email: <email>kurt.haas@ubc.ca</email></corresp><fn><p>This review was presented at the symposium <italic>Coupling cellular metabolism to neuronal signalling</italic>, which took place at Physiology 2014, the annual meeting of The Physiological Society, London, UK on 1 July 2014.</p></fn></author-notes><pub-date pub-type="ppub"><day>15</day><month>8</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>10</day><month>1</month><year>2015</year></pub-date><volume>593</volume><issue>Pt 16</issue><fpage>3471</fpage><lpage>3481</lpage><history><date date-type="received"><day>11</day><month>9</month><year>2014</year></date><date date-type="accepted"><day>21</day><month>12</month><year>2014</year></date></history><permissions><copyright-statement>© 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society</copyright-statement><copyright-year>2014</copyright-year></permissions><abstract><p>The classical view of mitochondria as housekeeping organelles acting in the background to simply maintain cellular energy demands has been challenged by mounting evidence of their direct and active participation in synaptic plasticity in neurons. Time-lapse imaging has revealed that mitochondria are motile in dendrites, with their localization and fusion and fission events regulated by synaptic activity. The positioning of mitochondria directly influences function of nearby synapses through multiple pathways including control over local concentrations of ATP, Ca<sup>2+</sup> and reactive oxygen species. Recent studies have also shown that mitochondrial protein cascades, classically associated with apoptosis, are involved in neural plasticity in healthy cells. These findings link mitochondria to the plasticity- and metaplasticity-associated activity-dependent transcription factor myocyte enhancer factor 2 (MEF2), further repositioning mitochondria as potential command centres for regulation of synaptic plasticity. Intriguingly, MEF2 and mitochondrial functions appear to be intricately intertwined, as MEF2 is a target of mitochondrial apoptotic caspases and, in turn, MEF2 regulates mitochondrial genome transcription essential for production of superoxidase and hydrogen peroxidase. Here, we review evidence supporting mitochondria as central organelles controlling the spatiotemporal expression of neuronal plasticity, and attempt to disentangle the MEF2–mitochondria relationship mediating these functions.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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