BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia
Intermittent hypoxia causes a form of serotonin-dependent synaptic plasticity in the spinal cord known as phrenic long-term facilitation (pLTF). Here we show that increased synthesis of brain-derived neurotrophic factor (BDNF) in the spinal cord is necessary and sufficient for pLTF in adult rats. We...
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| Veröffentlicht in: | Nature neuroscience 2004-01, Vol.7 (1), p.48-55 |
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| creator | Mitchell, Gordon S Baker-Herman, Tracy L Fuller, David D Bavis, Ryan W Zabka, Andrea G Golder, Francis J Doperalski, Nicholas J Johnson, Rebecca A Watters, Jyoti J |
| description | Intermittent hypoxia causes a form of serotonin-dependent synaptic plasticity in the spinal cord known as phrenic long-term facilitation (pLTF). Here we show that increased synthesis of brain-derived neurotrophic factor (BDNF) in the spinal cord is necessary and sufficient for pLTF in adult rats. We found that intermittent hypoxia elicited serotonin-dependent increases in BDNF synthesis in ventral spinal segments containing the phrenic nucleus, and the magnitude of these BDNF increases correlated with pLTF magnitude. We used RNA interference (RNAi) to interfere with BDNF expression, and tyrosine kinase receptor inhibition to block BDNF signaling. These disruptions blocked pLTF, whereas intrathecal injection of BDNF elicited an effect similar to pLTF. Our findings demonstrate new roles and regulatory mechanisms for BDNF in the spinal cord and suggest new therapeutic strategies for treating breathing disorders such as respiratory insufficiency after spinal injury. These experiments also illustrate the potential use of RNAi to investigate functional consequences of gene expression in the mammalian nervous system in vivo. |
| doi_str_mv | 10.1038/nn1166 |
| format | Article |
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Here we show that increased synthesis of brain-derived neurotrophic factor (BDNF) in the spinal cord is necessary and sufficient for pLTF in adult rats. We found that intermittent hypoxia elicited serotonin-dependent increases in BDNF synthesis in ventral spinal segments containing the phrenic nucleus, and the magnitude of these BDNF increases correlated with pLTF magnitude. We used RNA interference (RNAi) to interfere with BDNF expression, and tyrosine kinase receptor inhibition to block BDNF signaling. These disruptions blocked pLTF, whereas intrathecal injection of BDNF elicited an effect similar to pLTF. Our findings demonstrate new roles and regulatory mechanisms for BDNF in the spinal cord and suggest new therapeutic strategies for treating breathing disorders such as respiratory insufficiency after spinal injury. These experiments also illustrate the potential use of RNAi to investigate functional consequences of gene expression in the mammalian nervous system in vivo.</description><identifier>ISSN: 1097-6256</identifier><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/nn1166</identifier><identifier>PMID: 14699417</identifier><identifier>CODEN: NANEFN</identifier><language>eng</language><publisher>United States: Nature Publishing Group</publisher><subject>Animals ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - biosynthesis ; Genetic aspects ; Health aspects ; Hypoxia ; Hypoxia - metabolism ; Male ; Neuronal Plasticity - physiology ; Neuroplasticity ; Phrenic Nerve - metabolism ; Physiological aspects ; Rats ; Rats, Sprague-Dawley ; Respiration ; Spinal Cord - metabolism</subject><ispartof>Nature neuroscience, 2004-01, Vol.7 (1), p.48-55</ispartof><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-9f2947922e3bc47f89c108323264de13df5d543a54fa1ac1b63aa5e27bc9a1203</citedby><cites>FETCH-LOGICAL-c427t-9f2947922e3bc47f89c108323264de13df5d543a54fa1ac1b63aa5e27bc9a1203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14699417$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mitchell, Gordon S</creatorcontrib><creatorcontrib>Baker-Herman, Tracy L</creatorcontrib><creatorcontrib>Fuller, David D</creatorcontrib><creatorcontrib>Bavis, Ryan W</creatorcontrib><creatorcontrib>Zabka, Andrea G</creatorcontrib><creatorcontrib>Golder, Francis J</creatorcontrib><creatorcontrib>Doperalski, Nicholas J</creatorcontrib><creatorcontrib>Johnson, Rebecca A</creatorcontrib><creatorcontrib>Watters, Jyoti J</creatorcontrib><title>BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><description>Intermittent hypoxia causes a form of serotonin-dependent synaptic plasticity in the spinal cord known as phrenic long-term facilitation (pLTF). Here we show that increased synthesis of brain-derived neurotrophic factor (BDNF) in the spinal cord is necessary and sufficient for pLTF in adult rats. We found that intermittent hypoxia elicited serotonin-dependent increases in BDNF synthesis in ventral spinal segments containing the phrenic nucleus, and the magnitude of these BDNF increases correlated with pLTF magnitude. We used RNA interference (RNAi) to interfere with BDNF expression, and tyrosine kinase receptor inhibition to block BDNF signaling. These disruptions blocked pLTF, whereas intrathecal injection of BDNF elicited an effect similar to pLTF. Our findings demonstrate new roles and regulatory mechanisms for BDNF in the spinal cord and suggest new therapeutic strategies for treating breathing disorders such as respiratory insufficiency after spinal injury. 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Academic</collection><jtitle>Nature neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mitchell, Gordon S</au><au>Baker-Herman, Tracy L</au><au>Fuller, David D</au><au>Bavis, Ryan W</au><au>Zabka, Andrea G</au><au>Golder, Francis J</au><au>Doperalski, Nicholas J</au><au>Johnson, Rebecca A</au><au>Watters, Jyoti J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia</atitle><jtitle>Nature neuroscience</jtitle><addtitle>Nat Neurosci</addtitle><date>2004-01-01</date><risdate>2004</risdate><volume>7</volume><issue>1</issue><spage>48</spage><epage>55</epage><pages>48-55</pages><issn>1097-6256</issn><eissn>1546-1726</eissn><coden>NANEFN</coden><abstract>Intermittent hypoxia causes a form of serotonin-dependent synaptic plasticity in the spinal cord known as phrenic long-term facilitation (pLTF). Here we show that increased synthesis of brain-derived neurotrophic factor (BDNF) in the spinal cord is necessary and sufficient for pLTF in adult rats. We found that intermittent hypoxia elicited serotonin-dependent increases in BDNF synthesis in ventral spinal segments containing the phrenic nucleus, and the magnitude of these BDNF increases correlated with pLTF magnitude. We used RNA interference (RNAi) to interfere with BDNF expression, and tyrosine kinase receptor inhibition to block BDNF signaling. These disruptions blocked pLTF, whereas intrathecal injection of BDNF elicited an effect similar to pLTF. Our findings demonstrate new roles and regulatory mechanisms for BDNF in the spinal cord and suggest new therapeutic strategies for treating breathing disorders such as respiratory insufficiency after spinal injury. These experiments also illustrate the potential use of RNAi to investigate functional consequences of gene expression in the mammalian nervous system in vivo.</abstract><cop>United States</cop><pub>Nature Publishing Group</pub><pmid>14699417</pmid><doi>10.1038/nn1166</doi><tpages>8</tpages></addata></record> |
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| ispartof | Nature neuroscience, 2004-01, Vol.7 (1), p.48-55 |
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| subjects | Animals Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - biosynthesis Genetic aspects Health aspects Hypoxia Hypoxia - metabolism Male Neuronal Plasticity - physiology Neuroplasticity Phrenic Nerve - metabolism Physiological aspects Rats Rats, Sprague-Dawley Respiration Spinal Cord - metabolism |
| title | BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia |
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