Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression
The expression of high affinity neurotrophin receptors (TrkA, TrkB, and TrkC) determines the survival response of different populations of neurons to specific members of the neurotrophin family, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3)....
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| Veröffentlicht in: | FEBS letters 1994-12, Vol.356 (1), p.60-65 |
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| creator | Kobayashi, Miwako Kurihara, Kenzo Matsuoka, Ichiro |
| description | The expression of high affinity neurotrophin receptors (TrkA, TrkB, and TrkC) determines the survival response of different populations of neurons to specific members of the neurotrophin family, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3). However, the mechanism which controls the expression of neurotrophin receptors during neuronal development is largely unknown. Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of
trkA mRNA and induced the expression of
trkB mRNA. Expression of the functional TrkB receptor was confirmed by the emergence of trophic dependence of these neurons on BDNF in the absence of NGF. Differential regulation of
trk mRNAs by RA provides a possible model for the establishment of neurotrophin dependence of peripheral neurons. |
| doi_str_mv | 10.1016/0014-5793(94)01238-5 |
| format | Article |
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trkA mRNA and induced the expression of
trkB mRNA. Expression of the functional TrkB receptor was confirmed by the emergence of trophic dependence of these neurons on BDNF in the absence of NGF. Differential regulation of
trk mRNAs by RA provides a possible model for the establishment of neurotrophin dependence of peripheral neurons.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/0014-5793(94)01238-5</identifier><identifier>PMID: 7988722</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Animals ; BNDF, brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor ; Cell Survival ; Cells, Cultured ; Nerve Growth Factors - pharmacology ; Nerve Tissue Proteins - pharmacology ; Neurons - drug effects ; Neurons - metabolism ; Neurotrophin ; Neurotrophin receptor ; NGF, nerve growth factor ; NT-3, neurotrophin-3 ; Proto-Oncogene Proteins - biosynthesis ; RA, retinoc acid ; Rats ; Rats, Wistar ; Receptor Protein-Tyrosine Kinases - biosynthesis ; Receptor, Ciliary Neurotrophic Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor - biosynthesis ; Retinoic acid ; Reverse transcription-polymerase chain reaction ; RT-PCR, reverse transcription-polymerase chain reaction ; SCG, superior cervical ganglion ; Superior Cervical Ganglion - cytology ; Superior Cervical Ganglion - drug effects ; Superior Cervical Ganglion - metabolism ; Sympathetic Nervous System - cytology ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - metabolism ; Sympathetic neuron ; Tretinoin - pharmacology</subject><ispartof>FEBS letters, 1994-12, Vol.356 (1), p.60-65</ispartof><rights>1994</rights><rights>FEBS Letters 356 (1994) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5175-3e1ad0e3fe6cbbb9c461f79ddf20047c45c524e587032a04e446a05ba96fbad33</citedby><cites>FETCH-LOGICAL-c5175-3e1ad0e3fe6cbbb9c461f79ddf20047c45c524e587032a04e446a05ba96fbad33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0014579394012385$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7988722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kobayashi, Miwako</creatorcontrib><creatorcontrib>Kurihara, Kenzo</creatorcontrib><creatorcontrib>Matsuoka, Ichiro</creatorcontrib><title>Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>The expression of high affinity neurotrophin receptors (TrkA, TrkB, and TrkC) determines the survival response of different populations of neurons to specific members of the neurotrophin family, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3). However, the mechanism which controls the expression of neurotrophin receptors during neuronal development is largely unknown. Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of
trkA mRNA and induced the expression of
trkB mRNA. Expression of the functional TrkB receptor was confirmed by the emergence of trophic dependence of these neurons on BDNF in the absence of NGF. Differential regulation of
trk mRNAs by RA provides a possible model for the establishment of neurotrophin dependence of peripheral neurons.</description><subject>Animals</subject><subject>BNDF, brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Nerve Growth Factors - pharmacology</subject><subject>Nerve Tissue Proteins - pharmacology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurotrophin</subject><subject>Neurotrophin receptor</subject><subject>NGF, nerve growth factor</subject><subject>NT-3, neurotrophin-3</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>RA, retinoc acid</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor Protein-Tyrosine Kinases - biosynthesis</subject><subject>Receptor, Ciliary Neurotrophic Factor</subject><subject>Receptor, trkA</subject><subject>Receptors, Nerve Growth Factor - biosynthesis</subject><subject>Retinoic acid</subject><subject>Reverse transcription-polymerase chain reaction</subject><subject>RT-PCR, reverse transcription-polymerase chain reaction</subject><subject>SCG, superior cervical ganglion</subject><subject>Superior Cervical Ganglion - cytology</subject><subject>Superior Cervical Ganglion - drug effects</subject><subject>Superior Cervical Ganglion - metabolism</subject><subject>Sympathetic Nervous System - cytology</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Sympathetic neuron</subject><subject>Tretinoin - pharmacology</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EKtPCG4DkFYJFwI5_s0FqSweQKpBQWVuOfaMaMnGwk4F5-zrNqEtgZfmecz9b5yD0gpK3lFD5jhDKK6Ea9rrhbwitma7EI7ShWrGKcakfo82D5Sk6zfkHKXdNmxN0ohqtVV1v0P4bTGGIwWHrgsdh8LODjC8-fNniBHmMQw57GCBnHDucD7vRTrdlxeEB5lRU3B6w7SdIdgpxWEw36ecqTimOt2EoHAfjFBOGP2Nh5uJ7hp50ts_w_Hieoe_bq5vLT9X114-fL8-vKyeoEhUDaj0B1oF0bds2jkvaqcb7riaEK8eFEzUHoRVhtSUcOJeWiNY2smutZ-wMvVq5Y4q_ZsiT2YXsoO_tAHHORkmtOGXyn0YqFdVS6WLkq9GlmHOCzowp7Gw6GErM0otZQjdL6Kbh5r4XI8rayyN_bnfgH5aORRR9u-q_Qw-H_2Ka7dVFvQjLvOH30-Wh9ysISqz7AMlkF2Bw4EPpYTI-hr__9A6hQLJL</recordid><startdate>19941214</startdate><enddate>19941214</enddate><creator>Kobayashi, Miwako</creator><creator>Kurihara, Kenzo</creator><creator>Matsuoka, Ichiro</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>19941214</creationdate><title>Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression</title><author>Kobayashi, Miwako ; Kurihara, Kenzo ; Matsuoka, Ichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5175-3e1ad0e3fe6cbbb9c461f79ddf20047c45c524e587032a04e446a05ba96fbad33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>BNDF, brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Nerve Growth Factors - pharmacology</topic><topic>Nerve Tissue Proteins - pharmacology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurotrophin</topic><topic>Neurotrophin receptor</topic><topic>NGF, nerve growth factor</topic><topic>NT-3, neurotrophin-3</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>RA, retinoc acid</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor Protein-Tyrosine Kinases - biosynthesis</topic><topic>Receptor, Ciliary Neurotrophic Factor</topic><topic>Receptor, trkA</topic><topic>Receptors, Nerve Growth Factor - biosynthesis</topic><topic>Retinoic acid</topic><topic>Reverse transcription-polymerase chain reaction</topic><topic>RT-PCR, reverse transcription-polymerase chain reaction</topic><topic>SCG, superior cervical ganglion</topic><topic>Superior Cervical Ganglion - cytology</topic><topic>Superior Cervical Ganglion - drug effects</topic><topic>Superior Cervical Ganglion - metabolism</topic><topic>Sympathetic Nervous System - cytology</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Sympathetic neuron</topic><topic>Tretinoin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kobayashi, Miwako</creatorcontrib><creatorcontrib>Kurihara, Kenzo</creatorcontrib><creatorcontrib>Matsuoka, Ichiro</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>MEDLINE - Academic</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kobayashi, Miwako</au><au>Kurihara, Kenzo</au><au>Matsuoka, Ichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>1994-12-14</date><risdate>1994</risdate><volume>356</volume><issue>1</issue><spage>60</spage><epage>65</epage><pages>60-65</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>The expression of high affinity neurotrophin receptors (TrkA, TrkB, and TrkC) determines the survival response of different populations of neurons to specific members of the neurotrophin family, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3). However, the mechanism which controls the expression of neurotrophin receptors during neuronal development is largely unknown. Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of
trkA mRNA and induced the expression of
trkB mRNA. Expression of the functional TrkB receptor was confirmed by the emergence of trophic dependence of these neurons on BDNF in the absence of NGF. Differential regulation of
trk mRNAs by RA provides a possible model for the establishment of neurotrophin dependence of peripheral neurons.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>7988722</pmid><doi>10.1016/0014-5793(94)01238-5</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | FEBS letters, 1994-12, Vol.356 (1), p.60-65 |
| issn | 0014-5793 1873-3468 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete; Alma/SFX Local Collection; EZB* |
| subjects | Animals BNDF, brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor Cell Survival Cells, Cultured Nerve Growth Factors - pharmacology Nerve Tissue Proteins - pharmacology Neurons - drug effects Neurons - metabolism Neurotrophin Neurotrophin receptor NGF, nerve growth factor NT-3, neurotrophin-3 Proto-Oncogene Proteins - biosynthesis RA, retinoc acid Rats Rats, Wistar Receptor Protein-Tyrosine Kinases - biosynthesis Receptor, Ciliary Neurotrophic Factor Receptor, trkA Receptors, Nerve Growth Factor - biosynthesis Retinoic acid Reverse transcription-polymerase chain reaction RT-PCR, reverse transcription-polymerase chain reaction SCG, superior cervical ganglion Superior Cervical Ganglion - cytology Superior Cervical Ganglion - drug effects Superior Cervical Ganglion - metabolism Sympathetic Nervous System - cytology Sympathetic Nervous System - drug effects Sympathetic Nervous System - metabolism Sympathetic neuron Tretinoin - pharmacology |
| title | Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression |
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