trkB messenger RNA expression in normal human brain and in the substantia nigra of parkinsonian patients: an in situ hybridization study.
Identifieur interne : 001457 ( PubMed/Corpus ); précédent : 001456; suivant : 001458trkB messenger RNA expression in normal human brain and in the substantia nigra of parkinsonian patients: an in situ hybridization study.
Auteurs : S. Benisty ; F. Boissiere ; B. Faucheux ; Y. Agid ; E C HirschSource :
- Neuroscience [ 0306-4522 ] ; 1998.
English descriptors
- KwdEn :
- Autoradiography, Brain (metabolism), Cerebellum (metabolism), Cerebral Cortex (metabolism), Hippocampus (metabolism), Humans, In Situ Hybridization, Organ Specificity, Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), RNA, Messenger (genetics), Receptor Protein-Tyrosine Kinases (genetics), Receptor, Ciliary Neurotrophic Factor, Receptors, Nerve Growth Factor (genetics), Reference Values, Substantia Nigra (metabolism), Substantia Nigra (pathology), Sulfur Radioisotopes, Transcription, Genetic.
- MESH :
- chemical , genetics : RNA, Messenger, Receptor Protein-Tyrosine Kinases, Receptors, Nerve Growth Factor.
- genetics : Parkinson Disease.
- metabolism : Brain, Cerebellum, Cerebral Cortex, Hippocampus, Parkinson Disease, Substantia Nigra.
- pathology : Parkinson Disease, Substantia Nigra.
- Autoradiography, Humans, In Situ Hybridization, Organ Specificity, Receptor, Ciliary Neurotrophic Factor, Reference Values, Sulfur Radioisotopes, Transcription, Genetic.
Abstract
trkB is a high-affinity receptor for brain-derived neurotrophic factor, a neurotrophin acting on numerous cells, including dopaminergic neurons. Yet, little is known of its expression in the human brain. We report an in situ hybridization analysis of trkB messenger RNA, encoding the catalytic form of the receptor, in the human brain post mortem. Its expression was found to be widespread but heterogeneous among all the cerebral structures studied, the highest level being found in the cerebral cortex and the cerebellum. A strong but less intense staining was observed in the striatum, nucleus basalis of Meynert, hippocampus, tegmental pedonculopontinus nucleus and substantia nigra pars compacta. Combined immunohistochemistry for tyrosine hydroxylase and in situ hybridization for trkB messenger RNA showed that within the substantia nigra pars compacta a major proportion of dopaminergic neurons expressed trkB messenger RNA. Furthermore, we compared trkB messenger RNA expression in the mesencephalon of six control subjects and five patients with Parkinson's disease, a neurodegenerative disorder characterized by a severe loss of dopaminergic neurons. Despite the fact that the number of trkB messenger RNA-containing neurons was dramatically reduced in the substantia nigra pars compacta and ventral tegmental area of patients with Parkinson's disease, the level of trkB messenger RNA was unchanged in the remaining neurons in diseased brains. These results suggests that trkB is not involved in the process of neuronal death in Parkinson's disease. Furthermore, expression of brain-derived neurotrophic factor high-affinity receptor in patients could allow this neurotrophin to be used to prevent degeneration of surviving neurons at early stages of the disease.
PubMed: 9692719
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">trkB messenger RNA expression in normal human brain and in the substantia nigra of parkinsonian patients: an in situ hybridization study.</title><author><name sortKey="Benisty, S" sort="Benisty, S" uniqKey="Benisty S" first="S" last="Benisty">S. Benisty</name><affiliation><nlm:affiliation>INSERM U 289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Boissiere, F" sort="Boissiere, F" uniqKey="Boissiere F" first="F" last="Boissiere">F. Boissiere</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9692719</idno><idno type="pmid">9692719</idno><idno type="wicri:Area/PubMed/Corpus">001457</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001457</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">trkB messenger RNA expression in normal human brain and in the substantia nigra of parkinsonian patients: an in situ hybridization study.</title><author><name sortKey="Benisty, S" sort="Benisty, S" uniqKey="Benisty S" first="S" last="Benisty">S. Benisty</name><affiliation><nlm:affiliation>INSERM U 289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Boissiere, F" sort="Boissiere, F" uniqKey="Boissiere F" first="F" last="Boissiere">F. Boissiere</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></analytic><series><title level="j">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autoradiography</term><term>Brain (metabolism)</term><term>Cerebellum (metabolism)</term><term>Cerebral Cortex (metabolism)</term><term>Hippocampus (metabolism)</term><term>Humans</term><term>In Situ Hybridization</term><term>Organ Specificity</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>RNA, Messenger (genetics)</term><term>Receptor Protein-Tyrosine Kinases (genetics)</term><term>Receptor, Ciliary Neurotrophic Factor</term><term>Receptors, Nerve Growth Factor (genetics)</term><term>Reference Values</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Sulfur Radioisotopes</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Messenger</term><term>Receptor Protein-Tyrosine Kinases</term><term>Receptors, Nerve Growth Factor</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Cerebellum</term><term>Cerebral Cortex</term><term>Hippocampus</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autoradiography</term><term>Humans</term><term>In Situ Hybridization</term><term>Organ Specificity</term><term>Receptor, Ciliary Neurotrophic Factor</term><term>Reference Values</term><term>Sulfur Radioisotopes</term><term>Transcription, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">trkB is a high-affinity receptor for brain-derived neurotrophic factor, a neurotrophin acting on numerous cells, including dopaminergic neurons. Yet, little is known of its expression in the human brain. We report an in situ hybridization analysis of trkB messenger RNA, encoding the catalytic form of the receptor, in the human brain post mortem. Its expression was found to be widespread but heterogeneous among all the cerebral structures studied, the highest level being found in the cerebral cortex and the cerebellum. A strong but less intense staining was observed in the striatum, nucleus basalis of Meynert, hippocampus, tegmental pedonculopontinus nucleus and substantia nigra pars compacta. Combined immunohistochemistry for tyrosine hydroxylase and in situ hybridization for trkB messenger RNA showed that within the substantia nigra pars compacta a major proportion of dopaminergic neurons expressed trkB messenger RNA. Furthermore, we compared trkB messenger RNA expression in the mesencephalon of six control subjects and five patients with Parkinson's disease, a neurodegenerative disorder characterized by a severe loss of dopaminergic neurons. Despite the fact that the number of trkB messenger RNA-containing neurons was dramatically reduced in the substantia nigra pars compacta and ventral tegmental area of patients with Parkinson's disease, the level of trkB messenger RNA was unchanged in the remaining neurons in diseased brains. These results suggests that trkB is not involved in the process of neuronal death in Parkinson's disease. Furthermore, expression of brain-derived neurotrophic factor high-affinity receptor in patients could allow this neurotrophin to be used to prevent degeneration of surviving neurons at early stages of the disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9692719</PMID><DateCreated><Year>1998</Year><Month>10</Month><Day>29</Day></DateCreated><DateCompleted><Year>1998</Year><Month>10</Month><Day>29</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0306-4522</ISSN><JournalIssue CitedMedium="Print"><Volume>86</Volume><Issue>3</Issue><PubDate><Year>1998</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neuroscience</Title><ISOAbbreviation>Neuroscience</ISOAbbreviation></Journal><ArticleTitle>trkB messenger RNA expression in normal human brain and in the substantia nigra of parkinsonian patients: an in situ hybridization study.</ArticleTitle><Pagination><MedlinePgn>813-26</MedlinePgn></Pagination><Abstract><AbstractText>trkB is a high-affinity receptor for brain-derived neurotrophic factor, a neurotrophin acting on numerous cells, including dopaminergic neurons. Yet, little is known of its expression in the human brain. We report an in situ hybridization analysis of trkB messenger RNA, encoding the catalytic form of the receptor, in the human brain post mortem. Its expression was found to be widespread but heterogeneous among all the cerebral structures studied, the highest level being found in the cerebral cortex and the cerebellum. A strong but less intense staining was observed in the striatum, nucleus basalis of Meynert, hippocampus, tegmental pedonculopontinus nucleus and substantia nigra pars compacta. Combined immunohistochemistry for tyrosine hydroxylase and in situ hybridization for trkB messenger RNA showed that within the substantia nigra pars compacta a major proportion of dopaminergic neurons expressed trkB messenger RNA. Furthermore, we compared trkB messenger RNA expression in the mesencephalon of six control subjects and five patients with Parkinson's disease, a neurodegenerative disorder characterized by a severe loss of dopaminergic neurons. Despite the fact that the number of trkB messenger RNA-containing neurons was dramatically reduced in the substantia nigra pars compacta and ventral tegmental area of patients with Parkinson's disease, the level of trkB messenger RNA was unchanged in the remaining neurons in diseased brains. These results suggests that trkB is not involved in the process of neuronal death in Parkinson's disease. Furthermore, expression of brain-derived neurotrophic factor high-affinity receptor in patients could allow this neurotrophin to be used to prevent degeneration of surviving neurons at early stages of the disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Benisty</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>INSERM U 289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boissiere</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscience</MedlineTA><NlmUniqueID>7605074</NlmUniqueID><ISSNLinking>0306-4522</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020801">Receptor, Ciliary Neurotrophic Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017475">Receptors, Nerve Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013462">Sulfur Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D020794">Receptor Protein-Tyrosine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001345" MajorTopicYN="N">Autoradiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002531" MajorTopicYN="N">Cerebellum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017403" MajorTopicYN="N">In Situ Hybridization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009928" MajorTopicYN="N">Organ Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020794" MajorTopicYN="N">Receptor Protein-Tyrosine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020801" MajorTopicYN="N">Receptor, Ciliary Neurotrophic Factor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017475" MajorTopicYN="N">Receptors, Nerve Growth Factor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013462" MajorTopicYN="N">Sulfur Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>8</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>8</Month><Day>6</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>8</Month><Day>6</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9692719</ArticleId><ArticleId IdType="pii">S0306452298001262</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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