INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model
The pathogenic role of SOD1 mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the de...
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| Veröffentlicht in: | Scientific reports 2016-04, Vol.6 (1), p.24515-24515, Article 24515 |
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| creator | Benedetti, Lorena Ghilardi, Anna Rottoli, Elsa De Maglie, Marcella Prosperi, Laura Perego, Carla Baruscotti, Mirko Bucchi, Annalisa Del Giacco, Luca Francolini, Maura |
| description | The pathogenic role of
SOD1
mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the development of motor nerve circuitry and embryo behavior, and suggest that these alterations are prompted by interneuron and motor neuron hyperexcitability triggered by anomalies in the persistent pacemaker sodium current I
NaP
. The riluzole-induced modulation of I
NaP
reduced spinal neuron excitability, reverted the behavioral phenotypes and improved the deficits in motor nerve circuitry development, thus shedding new light on the use of riluzole in the management of ALS. Our findings provide a valid phenotype-based tool for unbiased
in vivo
drug screening that can be used to develop new therapies. |
| doi_str_mv | 10.1038/srep24515 |
| format | Article |
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SOD1
mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the development of motor nerve circuitry and embryo behavior, and suggest that these alterations are prompted by interneuron and motor neuron hyperexcitability triggered by anomalies in the persistent pacemaker sodium current I
NaP
. The riluzole-induced modulation of I
NaP
reduced spinal neuron excitability, reverted the behavioral phenotypes and improved the deficits in motor nerve circuitry development, thus shedding new light on the use of riluzole in the management of ALS. Our findings provide a valid phenotype-based tool for unbiased
in vivo
drug screening that can be used to develop new therapies.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep24515</identifier><identifier>PMID: 27079797</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/109 ; 13/44 ; 14/19 ; 14/28 ; 14/33 ; 14/63 ; 631/378/1689/1285 ; 631/378/87 ; 9/74 ; Action Potentials - drug effects ; Action Potentials - genetics ; Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - diagnosis ; Amyotrophic Lateral Sclerosis - genetics ; Animals ; Animals, Genetically Modified ; Disease Models, Animal ; Drug screening ; Excitability ; Gene Expression ; Humanities and Social Sciences ; Locomotion ; Motor Activity - drug effects ; Motor neurons ; Motor Neurons - drug effects ; Motor Neurons - physiology ; Motor task performance ; multidisciplinary ; Muscles - pathology ; Mutation ; Neuromuscular Junction - metabolism ; Phenotype ; Phenylglyoxal - analogs & derivatives ; Phenylglyoxal - pharmacology ; Riluzole - pharmacology ; Science ; Science (multidisciplinary) ; Sodium ; Spinal Cord - pathology ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Zebrafish</subject><ispartof>Scientific reports, 2016-04, Vol.6 (1), p.24515-24515, Article 24515</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Apr 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-c504t-610c9484191c3f2db1b29bdcb02c9bf0bc8c910ddd2ca4569c1d2e3094a7054a3</citedby><cites>FETCH-LOGICAL-c504t-610c9484191c3f2db1b29bdcb02c9bf0bc8c910ddd2ca4569c1d2e3094a7054a3</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/PMC4832213/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4832213/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27079797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Benedetti, Lorena</creatorcontrib><creatorcontrib>Ghilardi, Anna</creatorcontrib><creatorcontrib>Rottoli, Elsa</creatorcontrib><creatorcontrib>De Maglie, Marcella</creatorcontrib><creatorcontrib>Prosperi, Laura</creatorcontrib><creatorcontrib>Perego, Carla</creatorcontrib><creatorcontrib>Baruscotti, Mirko</creatorcontrib><creatorcontrib>Bucchi, Annalisa</creatorcontrib><creatorcontrib>Del Giacco, Luca</creatorcontrib><creatorcontrib>Francolini, Maura</creatorcontrib><title>INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The pathogenic role of
SOD1
mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the development of motor nerve circuitry and embryo behavior, and suggest that these alterations are prompted by interneuron and motor neuron hyperexcitability triggered by anomalies in the persistent pacemaker sodium current I
NaP
. The riluzole-induced modulation of I
NaP
reduced spinal neuron excitability, reverted the behavioral phenotypes and improved the deficits in motor nerve circuitry development, thus shedding new light on the use of riluzole in the management of ALS. Our findings provide a valid phenotype-based tool for unbiased
in vivo
drug screening that can be used to develop new therapies.</description><subject>13/1</subject><subject>13/109</subject><subject>13/44</subject><subject>14/19</subject><subject>14/28</subject><subject>14/33</subject><subject>14/63</subject><subject>631/378/1689/1285</subject><subject>631/378/87</subject><subject>9/74</subject><subject>Action Potentials - drug effects</subject><subject>Action Potentials - genetics</subject><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - diagnosis</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Disease Models, Animal</subject><subject>Drug screening</subject><subject>Excitability</subject><subject>Gene Expression</subject><subject>Humanities and Social Sciences</subject><subject>Locomotion</subject><subject>Motor Activity - drug effects</subject><subject>Motor neurons</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Benedetti, Lorena</au><au>Ghilardi, Anna</au><au>Rottoli, Elsa</au><au>De Maglie, Marcella</au><au>Prosperi, Laura</au><au>Perego, Carla</au><au>Baruscotti, Mirko</au><au>Bucchi, Annalisa</au><au>Del Giacco, Luca</au><au>Francolini, Maura</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-04-15</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>24515</spage><epage>24515</epage><pages>24515-24515</pages><artnum>24515</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The pathogenic role of
SOD1
mutations in amyotrophic lateral sclerosis (ALS) was investigated using a zebrafish disease model stably expressing the ALS-linked G93R mutation. In addition to the main pathological features of ALS shown by adult fish, we found remarkably precocious alterations in the development of motor nerve circuitry and embryo behavior, and suggest that these alterations are prompted by interneuron and motor neuron hyperexcitability triggered by anomalies in the persistent pacemaker sodium current I
NaP
. The riluzole-induced modulation of I
NaP
reduced spinal neuron excitability, reverted the behavioral phenotypes and improved the deficits in motor nerve circuitry development, thus shedding new light on the use of riluzole in the management of ALS. Our findings provide a valid phenotype-based tool for unbiased
in vivo
drug screening that can be used to develop new therapies.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27079797</pmid><doi>10.1038/srep24515</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/109 13/44 14/19 14/28 14/33 14/63 631/378/1689/1285 631/378/87 9/74 Action Potentials - drug effects Action Potentials - genetics Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - diagnosis Amyotrophic Lateral Sclerosis - genetics Animals Animals, Genetically Modified Disease Models, Animal Drug screening Excitability Gene Expression Humanities and Social Sciences Locomotion Motor Activity - drug effects Motor neurons Motor Neurons - drug effects Motor Neurons - physiology Motor task performance multidisciplinary Muscles - pathology Mutation Neuromuscular Junction - metabolism Phenotype Phenylglyoxal - analogs & derivatives Phenylglyoxal - pharmacology Riluzole - pharmacology Science Science (multidisciplinary) Sodium Spinal Cord - pathology Superoxide dismutase Superoxide Dismutase - genetics Zebrafish |
| title | INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model |
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