The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease
Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are widely expressed in the vertebrate nervous system and play a central role in mature neuronal function. In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults....
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| Veröffentlicht in: | Human molecular genetics 2011-11, Vol.20 (21), p.4116-4131 |
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| container_title | Human molecular genetics |
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| creator | Zhai, Jinbin Zhou, Weiguo Li, Jian Hayworth, Christopher R. Zhang, Lei Misawa, Hidemi Klein, Rudiger Scherer, Steven S. Balice-Gordon, Rita J. Kalb, Robert Gordon |
| description | Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are widely expressed in the vertebrate nervous system and play a central role in mature neuronal function. In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults. Paradoxically, BDNF/TrkB signaling has also been shown, under certain in vitro circumstances, to render neurons vulnerable to insults. We show here that in vivo conditional deletion of TrkB from mature motor neurons attenuates mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking motor neuron TrkB live a month longer than controls and retain motor function for a longer period, particularly in the early phase of the disease. These effects are subserved by slowed motor neuron loss, persistence of neuromuscular junction integrity and reduced astrocytic and microglial reactivity within the spinal cord. These results suggest that manipulation of BDNF/TrkB signaling might have therapeutic efficacy in motor neuron diseases. |
| doi_str_mv | 10.1093/hmg/ddr335 |
| format | Article |
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In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults. Paradoxically, BDNF/TrkB signaling has also been shown, under certain in vitro circumstances, to render neurons vulnerable to insults. We show here that in vivo conditional deletion of TrkB from mature motor neurons attenuates mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking motor neuron TrkB live a month longer than controls and retain motor function for a longer period, particularly in the early phase of the disease. These effects are subserved by slowed motor neuron loss, persistence of neuromuscular junction integrity and reduced astrocytic and microglial reactivity within the spinal cord. These results suggest that manipulation of BDNF/TrkB signaling might have therapeutic efficacy in motor neuron diseases.</description><identifier>ISSN: 0964-6906</identifier><identifier>EISSN: 1460-2083</identifier><identifier>DOI: 10.1093/hmg/ddr335</identifier><identifier>PMID: 21816949</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Amino Acid Substitution ; Animals ; Axons - metabolism ; Axons - pathology ; Biological and medical sciences ; Brain-derived neurotrophic factor ; Cell receptors ; Cell structures and functions ; Cell survival ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Denervation ; Disease Progression ; Fundamental and applied biological sciences. Psychology ; Ganglion Cysts - metabolism ; Ganglion Cysts - pathology ; Gene Deletion ; Genetics of eukaryotes. Biological and molecular evolution ; Inclusion Bodies - metabolism ; Inflammation - complications ; Inflammation - pathology ; Inflammation - physiopathology ; Integrases - metabolism ; Interneurons - metabolism ; Interneurons - pathology ; Longevity ; Medical sciences ; Mice ; Mice, Knockout ; Miscellaneous ; Molecular and cellular biology ; Motor Activity ; Motor neuron disease ; Motor Neuron Disease - complications ; Motor Neuron Disease - enzymology ; Motor Neuron Disease - pathology ; Motor Neuron Disease - physiopathology ; Motor Neurons - metabolism ; Motor Neurons - pathology ; Mutation - genetics ; Nervous system ; Neurology ; Neuromuscular Junction - metabolism ; Neuromuscular Junction - pathology ; Neuromuscular junctions ; Receptor mechanisms ; Receptor, trkB - metabolism ; Recombination, Genetic - genetics ; Spinal cord ; Spinal Cord - metabolism ; Spinal Cord - pathology ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase-1 ; Toxicity ; TrkB receptors ; Ubiquitin - metabolism ; Ubiquitination ; Vesicular Acetylcholine Transport Proteins - metabolism</subject><ispartof>Human molecular genetics, 2011-11, Vol.20 (21), p.4116-4131</ispartof><rights>The Author 2011. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-b9871842a167ed3cd5a793193812fdd94be2e11bd7ef49981ad0e23afed7ecd93</citedby><cites>FETCH-LOGICAL-c535t-b9871842a167ed3cd5a793193812fdd94be2e11bd7ef49981ad0e23afed7ecd93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24602937$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21816949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhai, Jinbin</creatorcontrib><creatorcontrib>Zhou, Weiguo</creatorcontrib><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Hayworth, Christopher R.</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Misawa, Hidemi</creatorcontrib><creatorcontrib>Klein, Rudiger</creatorcontrib><creatorcontrib>Scherer, Steven S.</creatorcontrib><creatorcontrib>Balice-Gordon, Rita J.</creatorcontrib><creatorcontrib>Kalb, Robert Gordon</creatorcontrib><title>The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease</title><title>Human molecular genetics</title><addtitle>Hum Mol Genet</addtitle><description>Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are widely expressed in the vertebrate nervous system and play a central role in mature neuronal function. In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults. Paradoxically, BDNF/TrkB signaling has also been shown, under certain in vitro circumstances, to render neurons vulnerable to insults. We show here that in vivo conditional deletion of TrkB from mature motor neurons attenuates mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking motor neuron TrkB live a month longer than controls and retain motor function for a longer period, particularly in the early phase of the disease. These effects are subserved by slowed motor neuron loss, persistence of neuromuscular junction integrity and reduced astrocytic and microglial reactivity within the spinal cord. These results suggest that manipulation of BDNF/TrkB signaling might have therapeutic efficacy in motor neuron diseases.</description><subject>Amino Acid Substitution</subject><subject>Animals</subject><subject>Axons - metabolism</subject><subject>Axons - pathology</subject><subject>Biological and medical sciences</subject><subject>Brain-derived neurotrophic factor</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Cell survival</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Denervation</subject><subject>Disease Progression</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ganglion Cysts - metabolism</subject><subject>Ganglion Cysts - pathology</subject><subject>Gene Deletion</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Inclusion Bodies - metabolism</subject><subject>Inflammation - complications</subject><subject>Inflammation - pathology</subject><subject>Inflammation - physiopathology</subject><subject>Integrases - metabolism</subject><subject>Interneurons - metabolism</subject><subject>Interneurons - pathology</subject><subject>Longevity</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Miscellaneous</subject><subject>Molecular and cellular biology</subject><subject>Motor Activity</subject><subject>Motor neuron disease</subject><subject>Motor Neuron Disease - complications</subject><subject>Motor Neuron Disease - enzymology</subject><subject>Motor Neuron Disease - pathology</subject><subject>Motor Neuron Disease - physiopathology</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - pathology</subject><subject>Mutation - genetics</subject><subject>Nervous system</subject><subject>Neurology</subject><subject>Neuromuscular Junction - metabolism</subject><subject>Neuromuscular Junction - pathology</subject><subject>Neuromuscular junctions</subject><subject>Receptor mechanisms</subject><subject>Receptor, trkB - metabolism</subject><subject>Recombination, Genetic - genetics</subject><subject>Spinal cord</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase-1</subject><subject>Toxicity</subject><subject>TrkB receptors</subject><subject>Ubiquitin - metabolism</subject><subject>Ubiquitination</subject><subject>Vesicular Acetylcholine Transport Proteins - metabolism</subject><issn>0964-6906</issn><issn>1460-2083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1LxDAQhoMouq5e_AGSiwhC3Xx02-Yi-K0geHA9eQhpMnWjbbMm7YL_3siuu3rxNMzMwzsfL0IHlJxSIvho2ryOjPGcjzfQgKYZSRgp-CYaEJGlSSZItoN2Q3gjhGYpz7fRDqMFzUQqBuhlMgVsWzy3c4e1aztvy76zrsWuwo3rnMct9D7mE_9-gT1omMViwJ3DTd-ptsNPj1f0L2psABVgD21Vqg6wv4xD9HxzPbm8Sx4eb-8vzx8SPebjLilFkdMiZYpmORiuzVjlglPBC8oqY0RaAgNKS5NDlQpRUGUIMK4qiBVtBB-is4XurC8bMBriFaqWM28b5T-lU1b-7bR2Kl_dXPL4hyxlUeB4KeDdRw-hk40NGupateD6IAUjuaCi-CZPFqT2LgQP1WoKJfLbDBnNkAszInz4e68V-vP9CBwtARW0qiuvWm3DmotWMsHzNef62X8DvwDJwqHf</recordid><startdate>20111101</startdate><enddate>20111101</enddate><creator>Zhai, Jinbin</creator><creator>Zhou, Weiguo</creator><creator>Li, Jian</creator><creator>Hayworth, Christopher R.</creator><creator>Zhang, Lei</creator><creator>Misawa, Hidemi</creator><creator>Klein, Rudiger</creator><creator>Scherer, Steven S.</creator><creator>Balice-Gordon, Rita J.</creator><creator>Kalb, Robert Gordon</creator><general>Oxford University Press</general><scope>IQODW</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20111101</creationdate><title>The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease</title><author>Zhai, Jinbin ; Zhou, Weiguo ; Li, Jian ; Hayworth, Christopher R. ; Zhang, Lei ; Misawa, Hidemi ; Klein, Rudiger ; Scherer, Steven S. ; Balice-Gordon, Rita J. ; Kalb, Robert Gordon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-b9871842a167ed3cd5a793193812fdd94be2e11bd7ef49981ad0e23afed7ecd93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Amino Acid Substitution</topic><topic>Animals</topic><topic>Axons - metabolism</topic><topic>Axons - pathology</topic><topic>Biological and medical sciences</topic><topic>Brain-derived neurotrophic factor</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Cell survival</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Denervation</topic><topic>Disease Progression</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ganglion Cysts - metabolism</topic><topic>Ganglion Cysts - pathology</topic><topic>Gene Deletion</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Inclusion Bodies - metabolism</topic><topic>Inflammation - complications</topic><topic>Inflammation - pathology</topic><topic>Inflammation - physiopathology</topic><topic>Integrases - metabolism</topic><topic>Interneurons - metabolism</topic><topic>Interneurons - pathology</topic><topic>Longevity</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Miscellaneous</topic><topic>Molecular and cellular biology</topic><topic>Motor Activity</topic><topic>Motor neuron disease</topic><topic>Motor Neuron Disease - complications</topic><topic>Motor Neuron Disease - enzymology</topic><topic>Motor Neuron Disease - pathology</topic><topic>Motor Neuron Disease - physiopathology</topic><topic>Motor Neurons - metabolism</topic><topic>Motor Neurons - pathology</topic><topic>Mutation - genetics</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Neuromuscular Junction - metabolism</topic><topic>Neuromuscular Junction - pathology</topic><topic>Neuromuscular junctions</topic><topic>Receptor mechanisms</topic><topic>Receptor, trkB - metabolism</topic><topic>Recombination, Genetic - genetics</topic><topic>Spinal cord</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase-1</topic><topic>Toxicity</topic><topic>TrkB receptors</topic><topic>Ubiquitin - metabolism</topic><topic>Ubiquitination</topic><topic>Vesicular Acetylcholine Transport Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhai, Jinbin</creatorcontrib><creatorcontrib>Zhou, Weiguo</creatorcontrib><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Hayworth, Christopher R.</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Misawa, Hidemi</creatorcontrib><creatorcontrib>Klein, Rudiger</creatorcontrib><creatorcontrib>Scherer, Steven S.</creatorcontrib><creatorcontrib>Balice-Gordon, Rita J.</creatorcontrib><creatorcontrib>Kalb, Robert Gordon</creatorcontrib><collection>Pascal-Francis</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human molecular genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhai, Jinbin</au><au>Zhou, Weiguo</au><au>Li, Jian</au><au>Hayworth, Christopher R.</au><au>Zhang, Lei</au><au>Misawa, Hidemi</au><au>Klein, Rudiger</au><au>Scherer, Steven S.</au><au>Balice-Gordon, Rita J.</au><au>Kalb, Robert Gordon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease</atitle><jtitle>Human molecular genetics</jtitle><addtitle>Hum Mol Genet</addtitle><date>2011-11-01</date><risdate>2011</risdate><volume>20</volume><issue>21</issue><spage>4116</spage><epage>4131</epage><pages>4116-4131</pages><issn>0964-6906</issn><eissn>1460-2083</eissn><abstract>Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are widely expressed in the vertebrate nervous system and play a central role in mature neuronal function. In vitro BDNF/TrkB signaling promotes neuronal survival and can help neurons resist toxic insults. Paradoxically, BDNF/TrkB signaling has also been shown, under certain in vitro circumstances, to render neurons vulnerable to insults. We show here that in vivo conditional deletion of TrkB from mature motor neurons attenuates mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking motor neuron TrkB live a month longer than controls and retain motor function for a longer period, particularly in the early phase of the disease. These effects are subserved by slowed motor neuron loss, persistence of neuromuscular junction integrity and reduced astrocytic and microglial reactivity within the spinal cord. These results suggest that manipulation of BDNF/TrkB signaling might have therapeutic efficacy in motor neuron diseases.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>21816949</pmid><doi>10.1093/hmg/ddr335</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Human molecular genetics, 2011-11, Vol.20 (21), p.4116-4131 |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Amino Acid Substitution Animals Axons - metabolism Axons - pathology Biological and medical sciences Brain-derived neurotrophic factor Cell receptors Cell structures and functions Cell survival Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Denervation Disease Progression Fundamental and applied biological sciences. Psychology Ganglion Cysts - metabolism Ganglion Cysts - pathology Gene Deletion Genetics of eukaryotes. Biological and molecular evolution Inclusion Bodies - metabolism Inflammation - complications Inflammation - pathology Inflammation - physiopathology Integrases - metabolism Interneurons - metabolism Interneurons - pathology Longevity Medical sciences Mice Mice, Knockout Miscellaneous Molecular and cellular biology Motor Activity Motor neuron disease Motor Neuron Disease - complications Motor Neuron Disease - enzymology Motor Neuron Disease - pathology Motor Neuron Disease - physiopathology Motor Neurons - metabolism Motor Neurons - pathology Mutation - genetics Nervous system Neurology Neuromuscular Junction - metabolism Neuromuscular Junction - pathology Neuromuscular junctions Receptor mechanisms Receptor, trkB - metabolism Recombination, Genetic - genetics Spinal cord Spinal Cord - metabolism Spinal Cord - pathology Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase-1 Toxicity TrkB receptors Ubiquitin - metabolism Ubiquitination Vesicular Acetylcholine Transport Proteins - metabolism |
| title | The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease |
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