Increased production of the TrkB protein tyrosine kinase receptor after brain insults
Identifieur interne : 004572 ( Main/Exploration ); précédent : 004571; suivant : 004573Increased production of the TrkB protein tyrosine kinase receptor after brain insults
Auteurs : Jean-Philippe Merlio [Suède, France] ; Patrik Ernfors [Suède] ; Zaal Kokaia [Suède] ; David S. Middlemas [États-Unis] ; Johan Bengzon [Suède] ; Merab Kokaia [Suède] ; Maj-Lis Smith [Suède] ; Bo K. Siesjö [Suède] ; Tony Hunter [États-Unis] ; Olle Lindvall [Suède] ; H Kan Persson [Suède]Source :
- 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
Affiliations:
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Middlemas</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Molecular Biology and Virology Laboratory The Salk Institute La Jolla</wicri:cityArea></affiliation></author><author><name sortKey="Bengzon, Johan" sort="Bengzon, Johan" uniqKey="Bengzon J" first="Johan" last="Bengzon">Johan Bengzon</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund</wicri:regionArea></affiliation></author><author><name sortKey="Kokaia, Merab" sort="Kokaia, Merab" uniqKey="Kokaia M" first="Merab" last="Kokaia">Merab Kokaia</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund</wicri:regionArea></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 wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund</wicri:regionArea></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 wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Laboratory for Experimental Brain Research University Hospital S-221 85 Lund</wicri:regionArea></affiliation></author><author><name sortKey="Hunter, Tony" sort="Hunter, Tony" uniqKey="Hunter T" first="Tony" last="Hunter">Tony Hunter</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Molecular Biology and Virology Laboratory The Salk Institute La Jolla</wicri:cityArea></affiliation></author><author><name sortKey="Lindvall, Olle" sort="Lindvall, Olle" uniqKey="Lindvall O" first="Olle" last="Lindvall">Olle Lindvall</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Restorative Neurology Unit Department of Neurology University Hospital S-221 85 Lund</wicri:regionArea></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 wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Medical Chemistry Laboratory of Molecular Neurobiology Karolinska Institute S-104 01 Stockholm</wicri:regionArea></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><affiliations><list><country><li>France</li><li>Suède</li><li>États-Unis</li></country><region><li>Aquitaine</li><li>Californie</li><li>Nouvelle-Aquitaine</li></region><settlement><li>Bordeaux</li></settlement></list><tree><country name="Suède"><noRegion><name sortKey="Merlio, Jean Philippe" sort="Merlio, Jean Philippe" uniqKey="Merlio J" first="Jean-Philippe" last="Merlio">Jean-Philippe Merlio</name></noRegion><name sortKey="Bengzon, Johan" sort="Bengzon, Johan" uniqKey="Bengzon J" first="Johan" last="Bengzon">Johan Bengzon</name><name sortKey="Ernfors, Patrik" sort="Ernfors, Patrik" uniqKey="Ernfors P" first="Patrik" last="Ernfors">Patrik Ernfors</name><name sortKey="Kokaia, Merab" sort="Kokaia, Merab" uniqKey="Kokaia M" first="Merab" last="Kokaia">Merab Kokaia</name><name sortKey="Kokaia, Zaal" sort="Kokaia, Zaal" uniqKey="Kokaia Z" first="Zaal" last="Kokaia">Zaal Kokaia</name><name sortKey="Lindvall, Olle" sort="Lindvall, Olle" uniqKey="Lindvall O" first="Olle" last="Lindvall">Olle Lindvall</name><name sortKey="Persson, H Kan" sort="Persson, H Kan" uniqKey="Persson H" first="H Kan" last="Persson">H Kan Persson</name><name sortKey="Siesjo, Bo K" sort="Siesjo, Bo K" uniqKey="Siesjo B" first="Bo K." last="Siesjö">Bo K. Siesjö</name><name sortKey="Smith, Maj Lis" sort="Smith, Maj Lis" uniqKey="Smith M" first="Maj-Lis" last="Smith">Maj-Lis Smith</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Merlio, Jean Philippe" sort="Merlio, Jean Philippe" uniqKey="Merlio J" first="Jean-Philippe" last="Merlio">Jean-Philippe Merlio</name></region></country><country name="États-Unis"><region name="Californie"><name sortKey="Middlemas, David S" sort="Middlemas, David S" uniqKey="Middlemas D" first="David S." last="Middlemas">David S. Middlemas</name></region><name sortKey="Hunter, Tony" sort="Hunter, Tony" uniqKey="Hunter T" first="Tony" last="Hunter">Tony Hunter</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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