Increased production of the TrkB protein tyrosine kinase receptor after brain insults
Identifieur interne : 002705 ( Istex/Corpus ); précédent : 002704; suivant : 002706Increased production of the TrkB protein tyrosine kinase receptor after brain insults
Auteurs : Jean-Philippe Merlio ; Patrik Ernfors ; Zaal Kokaia ; David S. Middlemas ; Johan Bengzon ; Merab Kokaia ; Maj-Lis Smith ; Bo K. Siesjö ; Tony Hunter ; Olle Lindvall ; H Kan PerssonSource :
- Neuron [ 0896-6273 ] ; 1993.
English descriptors
- Teeft :
- Acad, Bdnf, Bdnf mrna, Bdnf protein, Brain area, Brain areas, Brain insults, Cerebral ischemia, Coma, Computerized image analysis, Control animals, Control levels, Coronal sections, Dentate, Dentate gyrus, Detection limit, Ebendal, Electrical stimulation, Electrical stimulations, Encoding, Entire extracellular region, Ernfors, Extracellular, Extracellular region, Forebrain, Forebrain ischemia, Fulllength, Glucose, Granule, Granule cell layer, Granule cells, Gyrus, High affinity receptor, Hilar region, Hippocampal, Hippocampus, Hybridization, Hybridized, Hypoglycemic, Hypoglycemic coma, Hypoglycemic insults, Immunohistochemical staining, Immunoreactivity, Ischemia, Kaplan, Kinase, Kindling, Klein, Kokaia, Last stimulation, Lindvall, Middlemas, Mrna, Mrna encoding, Mrna expression, Natl, Nerve growth factor, Neuron, Neurotrophic, Neurotrophic factor, Neurotrophin, Neurotrophin receptor expression, Normal blood glucose levels, Northern blot analysis, Nucleus basalis, Oligonucleotide, Persson, Piriform, Piriform cortex, Preimmune serum, Probe, Proc, Pyramidal, Pyramidal cell layer, Pyramidal layer, Receptor, Recovery period, Research council, Same magnification, Seizure, Significant change, Similar increases, Transient increase, Trkb, Trkb immunoreactivity, Trkb mrna, Trkb mrnas, Trkb protein, Trkb proteins, Trkb receptor, Trkb receptors, Trkc, Trkc mrna, Trkc mrnas, Tyrosine, Tyrosine kinase receptor.
Abstract
Abstract: The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.
Url:
DOI: 10.1016/0896-6273(93)90307-D
Links to Exploration step
ISTEX:995645ECC645EFA0CED3D0EC9C140A5AC18C5ED0Le document en format XML
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Middlemas</name><affiliation><mods:affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</mods:affiliation></affiliation></author><author><name sortKey="Bengzon, Johan" sort="Bengzon, Johan" uniqKey="Bengzon J" first="Johan" last="Bengzon">Johan Bengzon</name><affiliation><mods:affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Kokaia, Merab" sort="Kokaia, Merab" uniqKey="Kokaia M" first="Merab" last="Kokaia">Merab Kokaia</name><affiliation><mods:affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Smith, Maj Lis" sort="Smith, Maj Lis" uniqKey="Smith M" first="Maj-Lis" last="Smith">Maj-Lis Smith</name><affiliation><mods:affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Siesjo, Bo K" sort="Siesjo, Bo K" uniqKey="Siesjo B" first="Bo K." last="Siesjö">Bo K. Siesjö</name><affiliation><mods:affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Hunter, Tony" sort="Hunter, Tony" uniqKey="Hunter T" first="Tony" last="Hunter">Tony Hunter</name><affiliation><mods:affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</mods:affiliation></affiliation></author><author><name sortKey="Lindvall, Olle" sort="Lindvall, Olle" uniqKey="Lindvall O" first="Olle" last="Lindvall">Olle Lindvall</name><affiliation><mods:affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Persson, H Kan" sort="Persson, H Kan" uniqKey="Persson H" first="H Kan" last="Persson">H Kan Persson</name><affiliation><mods:affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuron</title><title level="j" type="abbrev">NEURON</title><idno type="ISSN">0896-6273</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="151">151</biblScope><biblScope unit="page" to="164">164</biblScope></imprint><idno type="ISSN">0896-6273</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0896-6273</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acad</term><term>Bdnf</term><term>Bdnf mrna</term><term>Bdnf protein</term><term>Brain area</term><term>Brain areas</term><term>Brain insults</term><term>Cerebral ischemia</term><term>Coma</term><term>Computerized image analysis</term><term>Control animals</term><term>Control levels</term><term>Coronal sections</term><term>Dentate</term><term>Dentate gyrus</term><term>Detection limit</term><term>Ebendal</term><term>Electrical stimulation</term><term>Electrical stimulations</term><term>Encoding</term><term>Entire extracellular region</term><term>Ernfors</term><term>Extracellular</term><term>Extracellular region</term><term>Forebrain</term><term>Forebrain ischemia</term><term>Fulllength</term><term>Glucose</term><term>Granule</term><term>Granule cell layer</term><term>Granule cells</term><term>Gyrus</term><term>High affinity receptor</term><term>Hilar region</term><term>Hippocampal</term><term>Hippocampus</term><term>Hybridization</term><term>Hybridized</term><term>Hypoglycemic</term><term>Hypoglycemic coma</term><term>Hypoglycemic insults</term><term>Immunohistochemical staining</term><term>Immunoreactivity</term><term>Ischemia</term><term>Kaplan</term><term>Kinase</term><term>Kindling</term><term>Klein</term><term>Kokaia</term><term>Last stimulation</term><term>Lindvall</term><term>Middlemas</term><term>Mrna</term><term>Mrna encoding</term><term>Mrna expression</term><term>Natl</term><term>Nerve growth factor</term><term>Neuron</term><term>Neurotrophic</term><term>Neurotrophic factor</term><term>Neurotrophin</term><term>Neurotrophin receptor expression</term><term>Normal blood glucose levels</term><term>Northern blot analysis</term><term>Nucleus basalis</term><term>Oligonucleotide</term><term>Persson</term><term>Piriform</term><term>Piriform cortex</term><term>Preimmune serum</term><term>Probe</term><term>Proc</term><term>Pyramidal</term><term>Pyramidal cell layer</term><term>Pyramidal layer</term><term>Receptor</term><term>Recovery period</term><term>Research council</term><term>Same magnification</term><term>Seizure</term><term>Significant change</term><term>Similar increases</term><term>Transient increase</term><term>Trkb</term><term>Trkb immunoreactivity</term><term>Trkb mrna</term><term>Trkb mrnas</term><term>Trkb protein</term><term>Trkb proteins</term><term>Trkb receptor</term><term>Trkb receptors</term><term>Trkc</term><term>Trkc mrna</term><term>Trkc mrnas</term><term>Tyrosine</term><term>Tyrosine kinase receptor</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>mrna</json:string><json:string>trkb</json:string><json:string>receptor</json:string><json:string>hippocampus</json:string><json:string>dentate</json:string><json:string>gyrus</json:string><json:string>dentate gyrus</json:string><json:string>bdnf</json:string><json:string>ischemia</json:string><json:string>ernfors</json:string><json:string>trkb mrna</json:string><json:string>trkc</json:string><json:string>hypoglycemic</json:string><json:string>kinase</json:string><json:string>neurotrophic</json:string><json:string>coma</json:string><json:string>hybridization</json:string><json:string>hypoglycemic coma</json:string><json:string>persson</json:string><json:string>kindling</json:string><json:string>neuron</json:string><json:string>granule</json:string><json:string>encoding</json:string><json:string>hippocampal</json:string><json:string>last stimulation</json:string><json:string>control animals</json:string><json:string>nerve growth factor</json:string><json:string>neurotrophin</json:string><json:string>hilar region</json:string><json:string>lindvall</json:string><json:string>middlemas</json:string><json:string>trkb mrnas</json:string><json:string>immunoreactivity</json:string><json:string>trkb receptor</json:string><json:string>hybridized</json:string><json:string>neurotrophic factor</json:string><json:string>forebrain</json:string><json:string>extracellular</json:string><json:string>cerebral ischemia</json:string><json:string>piriform</json:string><json:string>acad</json:string><json:string>pyramidal layer</json:string><json:string>natl</json:string><json:string>trkb protein</json:string><json:string>bdnf mrna</json:string><json:string>same magnification</json:string><json:string>fulllength</json:string><json:string>electrical stimulations</json:string><json:string>granule cell layer</json:string><json:string>proc</json:string><json:string>ebendal</json:string><json:string>glucose</json:string><json:string>kokaia</json:string><json:string>oligonucleotide</json:string><json:string>klein</json:string><json:string>pyramidal</json:string><json:string>piriform cortex</json:string><json:string>nucleus basalis</json:string><json:string>trkc mrna</json:string><json:string>coronal sections</json:string><json:string>northern blot analysis</json:string><json:string>hypoglycemic insults</json:string><json:string>trkc mrnas</json:string><json:string>high affinity receptor</json:string><json:string>trkb receptors</json:string><json:string>recovery period</json:string><json:string>trkb proteins</json:string><json:string>entire extracellular region</json:string><json:string>extracellular region</json:string><json:string>seizure</json:string><json:string>kaplan</json:string><json:string>neurotrophin receptor expression</json:string><json:string>tyrosine kinase receptor</json:string><json:string>brain insults</json:string><json:string>brain areas</json:string><json:string>mrna expression</json:string><json:string>granule cells</json:string><json:string>immunohistochemical staining</json:string><json:string>trkb immunoreactivity</json:string><json:string>control levels</json:string><json:string>computerized image analysis</json:string><json:string>detection limit</json:string><json:string>mrna encoding</json:string><json:string>electrical stimulation</json:string><json:string>pyramidal cell layer</json:string><json:string>significant change</json:string><json:string>normal blood glucose levels</json:string><json:string>similar increases</json:string><json:string>preimmune serum</json:string><json:string>bdnf protein</json:string><json:string>brain area</json:string><json:string>forebrain ischemia</json:string><json:string>research council</json:string><json:string>transient increase</json:string><json:string>tyrosine</json:string><json:string>probe</json:string></teeft></keywords><author><json:item><name>Jean-Philippe Merlio</name><affiliations><json:string>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</json:string><json:string>† Present address: URA-CNRS 1200, Laboratoire d'HistologieEmbryologie Université de Bordeaux II, 33076, Bordeaux, France.</json:string></affiliations></json:item><json:item><name>Patrik Ernfors</name><affiliations><json:string>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>Zaal Kokaia</name><affiliations><json:string>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>David S. Middlemas</name><affiliations><json:string>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</json:string></affiliations></json:item><json:item><name>Johan Bengzon</name><affiliations><json:string>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>Merab Kokaia</name><affiliations><json:string>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>Maj-Lis Smith</name><affiliations><json:string>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>Bo K. Siesjö</name><affiliations><json:string>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>Tony Hunter</name><affiliations><json:string>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</json:string></affiliations></json:item><json:item><name>Olle Lindvall</name><affiliations><json:string>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</json:string></affiliations></json:item><json:item><name>Håkan Persson</name><affiliations><json:string>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-SNBSC1T3-H</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</abstract><qualityIndicators><score>8.884</score><pdfWordCount>6130</pdfWordCount><pdfCharCount>59187</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>14</pdfPageCount><pdfPageSize>576 x 864 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>157</abstractWordCount><abstractCharCount>1030</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Increased production of the TrkB protein tyrosine kinase receptor after brain insults</title><pmid><json:string>8439408</json:string></pmid><pii><json:string>0896-6273(93)90307-D</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. USA</title><language><json:string>unknown</json:string></language><volume>79</volume><pages><first>2519</first><last>2523</last></pages></serie><host><title>Neuron</title><language><json:string>unknown</json:string></language><publicationDate>1993</publicationDate><issn><json:string>0896-6273</json:string></issn><pii><json:string>S0896-6273(00)X0198-5</json:string></pii><volume>10</volume><issue>2</issue><pages><first>151</first><last>164</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1993</json:string><json:string>35S</json:string></date><geogName></geogName><orgName><json:string>Swedish Royal Academy of Sciences</json:string><json:string>Restorative Neurology Unit Department of Neurology University Hospital S</json:string><json:string>Lund Sweden Kokaia</json:string><json:string>Experimental Brain Research University Hospital S</json:string><json:string>Swedish Natural Science Research Council, the Swedish Medical Research Council, US</json:string><json:string>Recherche Medicale-Swedish Medical Research Council</json:string><json:string>University of Colorado</json:string><json:string>University of Wisconsin Genetic Computer Group</json:string><json:string>Apple Computer, Inc., Cupertino</json:string><json:string>Virology Laboratory The Salk Institute La Jolla, California</json:string><json:string>French Cancer Research Association</json:string><json:string>Breeding Center, Copenhagen, Denmark</json:string><json:string>Swedish Medical Research Council</json:string><json:string>Bank of Sweden TercentenaryFoundation</json:string><json:string>KonungGustavV</json:string></orgName><orgName_funder><json:string>Bank of Sweden TercentenaryFoundation</json:string><json:string>KonungGustavV</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Brain Res</json:string><json:string>Bo K. Siesjo</json:string><json:string>Lena Evergren</json:string><json:string>Time Course</json:string><json:string>Brain Detection</json:string><json:string>Wayne Rasband</json:string><json:string>Patrik Ernfors</json:string><json:string>Tony Hunter</json:string><json:string>Augusta Hedlunds</json:string><json:string>Elsa Segerfalks</json:string><json:string>Magnus Bergvalls</json:string><json:string>Lis Smith</json:string><json:string>David S. Middlemas</json:string><json:string>Agneta Othberg</json:string></persName><placeName><json:string>Lund</json:string><json:string>Uppsala</json:string><json:string>Bordeaux</json:string><json:string>Denmark</json:string><json:string>France</json:string><json:string>Copenhagen</json:string><json:string>Sweden</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Sanger et al., 1977</json:string><json:string>Middlemas, 1992</json:string><json:string>Klein et al., 1991b</json:string><json:string>Ernfors et al., 1988</json:string><json:string>Gall and Isackson, 1989</json:string><json:string>reviewed in Persson and Ernfors, 1993</json:string><json:string>DiStefano et al., 1992</json:string><json:string>Hohn et al., 1990</json:string><json:string>Radeke et al., 1987</json:string><json:string>Auer et al., 1984</json:string><json:string>Zafra et al., 1990</json:string><json:string>Banjeree et al., 1973</json:string><json:string>Phillips et al., 1990</json:string><json:string>Leibrock et al., 1989</json:string><json:string>Middlemas et al., 1991</json:string><json:string>Bengzon et al., 1992</json:string><json:string>Klein et al., 1991a</json:string><json:string>Buzsaki et al., 1989</json:string><json:string>Berkemeier et al., 1991</json:string><json:string>Dugich-Djordjevic et al., 1992</json:string><json:string>Lamballe et al., 1991</json:string><json:string>Shigeno et al., 1991</json:string><json:string>Barde et al., 1982</json:string><json:string>Klein et al., 1991</json:string><json:string>Johnson et al., 1986</json:string><json:string>Thoenen et al., 1987</json:string><json:string>Soppet et al., 1991</json:string><json:string>Jones and Reichardt, 1990</json:string><json:string>Whittemore and Seiger, 1987</json:string><json:string>Rosenthal et al., 1990</json:string><json:string>Martin-Zanca et al., 1989</json:string><json:string>Cheng and Mattson, 1991</json:string><json:string>Seiler et al., 1984</json:string><json:string>Kaisho et al., 1990</json:string><json:string>Sutter et al., 1979</json:string><json:string>Hallbook et al., 1991</json:string><json:string>Merlio et al. 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(1989)</json:string><json:string>Ernfors et al., 1990b</json:string><json:string>Ernfors et al., 1990a, 1990b</json:string><json:string>Lindvall et al., 1992</json:string><json:string>Ayer-LeLievre et al., 1988</json:string><json:string>Clark et al., 1985</json:string><json:string>Ernfors et al., 1991</json:string><json:string>Klein et al., 1989</json:string><json:string>Lothman et al., 1985</json:string><json:string>Hsu et al., 1981</json:string><json:string>Ip et al., 1992</json:string><json:string>Klein et al., 1989, 1990</json:string><json:string>Ernfors et al., 1990a</json:string><json:string>Schwab et al., 1979</json:string><json:string>Herrup and Shooter, 1973</json:string><json:string>Gall et al., 1991</json:string><json:string>Wetmore et al., 1990</json:string><json:string>Kaplan et al. (1991a, 1991b)</json:string><json:string>Smith et al., 1984</json:string><json:string>Hofer et al., 1990</json:string><json:string>reviewed in Ullrich and Schlessinger, 1990</json:string><json:string>Shaw and Kamen, 1986</json:string><json:string>RodriguezTebar et al., 1990</json:string><json:string>Hempstead et al., 1991</json:string><json:string>Kaplan et al., 1991a, 1991b</json:string><json:string>Ibanez et al., 1992</json:string><json:string>Ernfors et al., 1989</json:string><json:string>Morgan and Curran, 1991</json:string><json:string>Maisonpierre et al., 1990</json:string><json:string>Devereux et al., 1984</json:string><json:string>Klein et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-SNBSC1T3-H</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - neurosciences</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - neurology & neurosurgery</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - General Neuroscience</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - traumatismes. maladies dues aux agents physiques</json:string></inist></categories><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1016/0896-6273(93)90307-D</json:string></doi><id>995645ECC645EFA0CED3D0EC9C140A5AC18C5ED0</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SNBSC1T3-H/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SNBSC1T3-H/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-SNBSC1T3-H/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Increased production of the TrkB protein tyrosine kinase receptor after brain insults</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1993</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Increased production of the TrkB protein tyrosine kinase receptor after brain insults</title><author xml:id="author-0000"><persName><forename type="first">Jean-Philippe</forename><surname>Merlio</surname></persName><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation><affiliation>† Present address: URA-CNRS 1200, Laboratoire d'HistologieEmbryologie Université de Bordeaux II, 33076, Bordeaux, France.</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Patrik</forename><surname>Ernfors</surname></persName><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Zaal</forename><surname>Kokaia</surname></persName><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0003"><persName><forename type="first">David S.</forename><surname>Middlemas</surname></persName><affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Johan</forename><surname>Bengzon</surname></persName><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Merab</forename><surname>Kokaia</surname></persName><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Maj-Lis</forename><surname>Smith</surname></persName><affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Bo K.</forename><surname>Siesjö</surname></persName><affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0008"><persName><forename type="first">Tony</forename><surname>Hunter</surname></persName><affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</affiliation></author><author xml:id="author-0009"><persName><forename type="first">Olle</forename><surname>Lindvall</surname></persName><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation></author><author xml:id="author-0010"><persName><forename type="first">Håkan</forename><surname>Persson</surname></persName><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation></author><idno type="istex">995645ECC645EFA0CED3D0EC9C140A5AC18C5ED0</idno><idno type="ark">ark:/67375/6H6-SNBSC1T3-H</idno><idno type="DOI">10.1016/0896-6273(93)90307-D</idno><idno type="PII">0896-6273(93)90307-D</idno></analytic><monogr><title level="j">Neuron</title><title level="j" type="abbrev">NEURON</title><idno type="pISSN">0896-6273</idno><idno type="PII">S0896-6273(00)X0198-5</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">10</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="151">151</biblScope><biblScope unit="page" to="164">164</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</p></abstract></profileDesc><revisionDesc><change when="1992-10-14">Modified</change><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SNBSC1T3-H/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>NEURON</jid><aid>9390307D</aid><ce:pii>0896-6273(93)90307-D</ce:pii><ce:doi>10.1016/0896-6273(93)90307-D</ce:doi><ce:copyright type="unknown" year="1993"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Increased production of the TrkB protein tyrosine kinase receptor after brain insults</ce:title><ce:author-group><ce:author><ce:given-name>Jean-Philippe</ce:given-name><ce:surname>Merlio</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Patrik</ce:given-name><ce:surname>Ernfors</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Zaal</ce:given-name><ce:surname>Kokaia</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>David S.</ce:given-name><ce:surname>Middlemas</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Johan</ce:given-name><ce:surname>Bengzon</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Merab</ce:given-name><ce:surname>Kokaia</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Maj-Lis</ce:given-name><ce:surname>Smith</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>∥</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Bo K.</ce:given-name><ce:surname>Siesjö</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>∥</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tony</ce:given-name><ce:surname>Hunter</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Olle</ce:given-name><ce:surname>Lindvall</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Håkan</ce:given-name><ce:surname>Persson</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>†</ce:label><ce:note-para>Present address: URA-CNRS 1200, Laboratoire d'HistologieEmbryologie Université de Bordeaux II, 33076, Bordeaux, France.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="4" month="8" year="1992"></ce:date-received><ce:date-revised day="14" month="10" year="1992"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of <ce:italic>trk</ce:italic>B mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. <ce:italic>trk</ce:italic>B mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on <ce:italic>trk</ce:italic> and <ce:italic>trk</ce:italic>C mRNAs. The increase in <ce:italic>trk</ce:italic>B m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Increased production of the TrkB protein tyrosine kinase receptor after brain insults</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Increased production of the TrkB protein tyrosine kinase receptor after brain insults</title></titleInfo><name type="personal"><namePart type="given">Jean-Philippe</namePart><namePart type="family">Merlio</namePart><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation><affiliation>† Present address: URA-CNRS 1200, Laboratoire d'HistologieEmbryologie Université de Bordeaux II, 33076, Bordeaux, France.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrik</namePart><namePart type="family">Ernfors</namePart><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zaal</namePart><namePart type="family">Kokaia</namePart><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David S.</namePart><namePart type="family">Middlemas</namePart><affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johan</namePart><namePart type="family">Bengzon</namePart><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Merab</namePart><namePart type="family">Kokaia</namePart><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maj-Lis</namePart><namePart type="family">Smith</namePart><affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bo K.</namePart><namePart type="family">Siesjö</namePart><affiliation>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tony</namePart><namePart type="family">Hunter</namePart><affiliation>Molecular Biology and Virology Laboratory The Salk Institute La Jolla, California 92037 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olle</namePart><namePart type="family">Lindvall</namePart><affiliation>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Håkan</namePart><namePart type="family">Persson</namePart><affiliation>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><dateModified encoding="w3cdtf">1992-10-14</dateModified><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB m NA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</abstract><note type="content">Section title: Article</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><titleInfo type="abbreviated"><title>NEURON</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued></originInfo><identifier type="ISSN">0896-6273</identifier><identifier type="PII">S0896-6273(00)X0198-5</identifier><part><date>1993</date><detail type="volume"><number>10</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>115</start><end>334</end></extent><extent unit="pages"><start>151</start><end>164</end></extent></part></relatedItem><identifier type="istex">995645ECC645EFA0CED3D0EC9C140A5AC18C5ED0</identifier><identifier type="ark">ark:/67375/6H6-SNBSC1T3-H</identifier><identifier type="DOI">10.1016/0896-6273(93)90307-D</identifier><identifier type="PII">0896-6273(93)90307-D</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SNBSC1T3-H/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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