Ciliary Neurotrophic Factor Protects Striatal Output Neurons in an Animal Model of Huntington Disease
Huntington disease is a dominantly inherited, untreatable neurological disorder featuring a progressive loss of striatal output neurons that results in dyskinesia, cognitive decline, and, ultimately, death. Neurotrophic factors have recently been shown to be protective in several animal models of ne...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1996-07, Vol.93 (14), p.7346-7351 |
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| creator | Anderson, Keith D. Panayotatos, Nikos Corcoran, Thomas L. Lindsay, Ronald M. Wiegand, Stanley J. |
| description | Huntington disease is a dominantly inherited, untreatable neurological disorder featuring a progressive loss of striatal output neurons that results in dyskinesia, cognitive decline, and, ultimately, death. Neurotrophic factors have recently been shown to be protective in several animal models of neurodegenerative disease, raising the possibility that such substances might also sustain the survival of compromised striatal output neurons. We determined whether intracerebral administration of brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could protect striatal output neurons in a rodent model of Huntington disease. Whereas treatment with brain-derived neurotrophic factor, nerve growth factor, or neurotrophin-3 provided no protection of striatal output neurons from death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate receptor agonist, treatment with ciliary neurotrophic factor afforded marked protection against this neurodegenerative insult. |
| doi_str_mv | 10.1073/pnas.93.14.7346 |
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Neurotrophic factors have recently been shown to be protective in several animal models of neurodegenerative disease, raising the possibility that such substances might also sustain the survival of compromised striatal output neurons. We determined whether intracerebral administration of brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could protect striatal output neurons in a rodent model of Huntington disease. Whereas treatment with brain-derived neurotrophic factor, nerve growth factor, or neurotrophin-3 provided no protection of striatal output neurons from death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate receptor agonist, treatment with ciliary neurotrophic factor afforded marked protection against this neurodegenerative insult.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.93.14.7346</identifier><identifier>PMID: 8692996</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Animal models ; Animals ; Brain ; Brain-Derived Neurotrophic Factor ; Catheterization ; Cell Death - drug effects ; Ciliary Neurotrophic Factor ; Corpus Striatum - drug effects ; Corpus Striatum - pathology ; Disease ; Disease Models, Animal ; Humans ; Huntington disease ; Huntington Disease - drug therapy ; Huntington Disease - pathology ; Injections ; Interneurons ; Nerve Growth Factors - pharmacology ; Nerve Tissue Proteins - pharmacology ; Nervous system ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - pathology ; Neuroscience ; Neurotrophin 3 ; Pumps ; Quinolinic Acid - toxicity ; Rats ; Receptors ; Recombinant Proteins - pharmacology ; Rodents</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1996-07, Vol.93 (14), p.7346-7351</ispartof><rights>Copyright 1996 National Academy of Sciences</rights><rights>Copyright National Academy of Sciences Jul 9, 1996</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c584t-491a2bebe43e19cc534570720a17d1e2f36c11efe18af491889607d7143528d73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/93/14.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/39588$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/39588$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8692996$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Anderson, Keith D.</creatorcontrib><creatorcontrib>Panayotatos, Nikos</creatorcontrib><creatorcontrib>Corcoran, Thomas L.</creatorcontrib><creatorcontrib>Lindsay, Ronald M.</creatorcontrib><creatorcontrib>Wiegand, Stanley J.</creatorcontrib><title>Ciliary Neurotrophic Factor Protects Striatal Output Neurons in an Animal Model of Huntington Disease</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Huntington disease is a dominantly inherited, untreatable neurological disorder featuring a progressive loss of striatal output neurons that results in dyskinesia, cognitive decline, and, ultimately, death. Neurotrophic factors have recently been shown to be protective in several animal models of neurodegenerative disease, raising the possibility that such substances might also sustain the survival of compromised striatal output neurons. We determined whether intracerebral administration of brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could protect striatal output neurons in a rodent model of Huntington disease. Whereas treatment with brain-derived neurotrophic factor, nerve growth factor, or neurotrophin-3 provided no protection of striatal output neurons from death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate receptor agonist, treatment with ciliary neurotrophic factor afforded marked protection against this neurodegenerative insult.</description><subject>Animal models</subject><subject>Animals</subject><subject>Brain</subject><subject>Brain-Derived Neurotrophic Factor</subject><subject>Catheterization</subject><subject>Cell Death - drug effects</subject><subject>Ciliary Neurotrophic Factor</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - pathology</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Humans</subject><subject>Huntington disease</subject><subject>Huntington Disease - drug therapy</subject><subject>Huntington Disease - pathology</subject><subject>Injections</subject><subject>Interneurons</subject><subject>Nerve Growth Factors - pharmacology</subject><subject>Nerve Tissue Proteins - pharmacology</subject><subject>Nervous system</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - pathology</subject><subject>Neuroscience</subject><subject>Neurotrophin 3</subject><subject>Pumps</subject><subject>Quinolinic Acid - toxicity</subject><subject>Rats</subject><subject>Receptors</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Rodents</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ksFrFDEUxoModa2eBUEJHvQ022SSmSTgpWytFaoV1HPIZt60WWaTaZKR9r83w66L9eDpwft-3-MLXxB6ScmSEsFORm_SUrEl5UvBePsILShRtGq5Io_RgpBaVJLX_Cl6ltKGEKIaSY7QkWxVrVS7QLBygzPxHn-FKYYcw3jjLD43NoeIv5UN2Jzw9xydyWbAV1Mep7yDfcLOY-PxqXfbon0JHQw49Phi8tn56xw8PnMJTILn6ElvhgQv9vMY_Tz_-GN1UV1effq8Or2sbCN5rriipl7DGjgDqqxtGG8EETUxVHQU6p61llLogUrTF1hK1RLRCcpZU8tOsGP0YXd3nNZb6Cz4HM2gx1gCxnsdjNMPFe9u9HX4pZlUcra_29tjuJ0gZb11ycIwGA9hSpo2LeFcqgK-_QfchCn68jRdE8qoaGRToJMdZGNIKUJ_yEGJnsvTc3laMU25nssrjtd_xz_w-7aK_mavz8Y_6oMD7_8L6H4ahgx3uZCvduQmlaYPKCv_Q7LfFEm31Q</recordid><startdate>19960709</startdate><enddate>19960709</enddate><creator>Anderson, Keith D.</creator><creator>Panayotatos, Nikos</creator><creator>Corcoran, Thomas L.</creator><creator>Lindsay, Ronald M.</creator><creator>Wiegand, Stanley J.</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>19960709</creationdate><title>Ciliary Neurotrophic Factor Protects Striatal Output Neurons in an Animal Model of Huntington Disease</title><author>Anderson, Keith D. ; Panayotatos, Nikos ; Corcoran, Thomas L. ; Lindsay, Ronald M. ; Wiegand, Stanley J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-491a2bebe43e19cc534570720a17d1e2f36c11efe18af491889607d7143528d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Brain</topic><topic>Brain-Derived Neurotrophic Factor</topic><topic>Catheterization</topic><topic>Cell Death - drug effects</topic><topic>Ciliary Neurotrophic Factor</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - pathology</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Humans</topic><topic>Huntington disease</topic><topic>Huntington Disease - drug therapy</topic><topic>Huntington Disease - pathology</topic><topic>Injections</topic><topic>Interneurons</topic><topic>Nerve Growth Factors - pharmacology</topic><topic>Nerve Tissue Proteins - pharmacology</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - pathology</topic><topic>Neuroscience</topic><topic>Neurotrophin 3</topic><topic>Pumps</topic><topic>Quinolinic Acid - toxicity</topic><topic>Rats</topic><topic>Receptors</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Anderson, Keith D.</creatorcontrib><creatorcontrib>Panayotatos, Nikos</creatorcontrib><creatorcontrib>Corcoran, Thomas L.</creatorcontrib><creatorcontrib>Lindsay, Ronald M.</creatorcontrib><creatorcontrib>Wiegand, Stanley J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Anderson, Keith D.</au><au>Panayotatos, Nikos</au><au>Corcoran, Thomas L.</au><au>Lindsay, Ronald M.</au><au>Wiegand, Stanley J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ciliary Neurotrophic Factor Protects Striatal Output Neurons in an Animal Model of Huntington Disease</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1996-07-09</date><risdate>1996</risdate><volume>93</volume><issue>14</issue><spage>7346</spage><epage>7351</epage><pages>7346-7351</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Huntington disease is a dominantly inherited, untreatable neurological disorder featuring a progressive loss of striatal output neurons that results in dyskinesia, cognitive decline, and, ultimately, death. Neurotrophic factors have recently been shown to be protective in several animal models of neurodegenerative disease, raising the possibility that such substances might also sustain the survival of compromised striatal output neurons. We determined whether intracerebral administration of brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3, or ciliary neurotrophic factor could protect striatal output neurons in a rodent model of Huntington disease. Whereas treatment with brain-derived neurotrophic factor, nerve growth factor, or neurotrophin-3 provided no protection of striatal output neurons from death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate receptor agonist, treatment with ciliary neurotrophic factor afforded marked protection against this neurodegenerative insult.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>8692996</pmid><doi>10.1073/pnas.93.14.7346</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animal models Animals Brain Brain-Derived Neurotrophic Factor Catheterization Cell Death - drug effects Ciliary Neurotrophic Factor Corpus Striatum - drug effects Corpus Striatum - pathology Disease Disease Models, Animal Humans Huntington disease Huntington Disease - drug therapy Huntington Disease - pathology Injections Interneurons Nerve Growth Factors - pharmacology Nerve Tissue Proteins - pharmacology Nervous system Neurology Neurons Neurons - drug effects Neurons - pathology Neuroscience Neurotrophin 3 Pumps Quinolinic Acid - toxicity Rats Receptors Recombinant Proteins - pharmacology Rodents |
| title | Ciliary Neurotrophic Factor Protects Striatal Output Neurons in an Animal Model of Huntington Disease |
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