Sensitization of the striatal dopaminergic system induced by chronic administration of a glutamate antagonist in the rat.
Identifieur interne : 001527 ( PubMed/Corpus ); précédent : 001526; suivant : 001528Sensitization of the striatal dopaminergic system induced by chronic administration of a glutamate antagonist in the rat.
Auteurs : B. Lannes ; G. MichelettiSource :
- Neuroscience and biobehavioral reviews [ 0149-7634 ] ; 1997.
English descriptors
- KwdEn :
- Animals, Behavior, Animal (drug effects), Blotting, Northern, Dizocilpine Maleate (pharmacology), Dopamine (metabolism), Dopamine (physiology), Excitatory Amino Acid Antagonists (pharmacology), In Situ Hybridization, Male, Neostriatum (drug effects), Neostriatum (metabolism), Neostriatum (physiology), Neurons (drug effects), Neurons (metabolism), Parkinson Disease, Secondary (physiopathology), RNA, Messenger (biosynthesis), Rats, Receptors, Dopamine D2 (biosynthesis), Receptors, Dopamine D2 (drug effects).
- MESH :
- chemical , biosynthesis : RNA, Messenger, Receptors, Dopamine D2.
- chemical , drug effects : Receptors, Dopamine D2.
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Dizocilpine Maleate, Excitatory Amino Acid Antagonists.
- drug effects : Behavior, Animal, Neostriatum, Neurons.
- metabolism : Neostriatum, Neurons.
- chemical , physiology : Dopamine, Neostriatum.
- physiopathology : Parkinson Disease, Secondary.
- Animals, Blotting, Northern, In Situ Hybridization, Male, Rats.
Abstract
The aim of the present study was to assess in the rat the pharmacological, biochemical and molecular (including in situ hybridization) consequences in the striatum of a prolonged (50 days) treatment with dizocilpine maleate (MK-801), an N-methyl-D-aspartate (NMDA) antagonist. We observed a sensitization-like effect characterized by a behavioural hyperresponsiveness to an acute injection of haloperidol (0.25 mg/kg), a dopaminergic antagonist. In rats chronically treated with MK-801, this hyperresponsiveness was associated with an increased D2 receptor (D2R) density in the striatum. At the transcriptional level, the D2R mRNA was also enhanced in the striatum. Quantitative in situ hybridization studies revealed that the number of neurons expressing the D2R mRNA was significantly enhanced in treated rats, whereas the mean amount of message per cell was unchanged. These changes could represent the neurobiological substrate of the observed sensitization. These results suggest that the D2R gene is under glutamate control via NMDA receptor in striatal neurons.
PubMed: 9195599
Links to Exploration step
pubmed:9195599Le document en format XML
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We observed a sensitization-like effect characterized by a behavioural hyperresponsiveness to an acute injection of haloperidol (0.25 mg/kg), a dopaminergic antagonist. In rats chronically treated with MK-801, this hyperresponsiveness was associated with an increased D2 receptor (D2R) density in the striatum. At the transcriptional level, the D2R mRNA was also enhanced in the striatum. Quantitative in situ hybridization studies revealed that the number of neurons expressing the D2R mRNA was significantly enhanced in treated rats, whereas the mean amount of message per cell was unchanged. These changes could represent the neurobiological substrate of the observed sensitization. These results suggest that the D2R gene is under glutamate control via NMDA receptor in striatal neurons.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9195599</PMID><DateCreated><Year>1997</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>1997</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0149-7634</ISSN><JournalIssue CitedMedium="Print"><Volume>21</Volume><Issue>4</Issue><PubDate><Year>1997</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Neuroscience and biobehavioral reviews</Title><ISOAbbreviation>Neurosci Biobehav Rev</ISOAbbreviation></Journal><ArticleTitle>Sensitization of the striatal dopaminergic system induced by chronic administration of a glutamate antagonist in the rat.</ArticleTitle><Pagination><MedlinePgn>417-24</MedlinePgn></Pagination><Abstract><AbstractText>The aim of the present study was to assess in the rat the pharmacological, biochemical and molecular (including in situ hybridization) consequences in the striatum of a prolonged (50 days) treatment with dizocilpine maleate (MK-801), an N-methyl-D-aspartate (NMDA) antagonist. We observed a sensitization-like effect characterized by a behavioural hyperresponsiveness to an acute injection of haloperidol (0.25 mg/kg), a dopaminergic antagonist. In rats chronically treated with MK-801, this hyperresponsiveness was associated with an increased D2 receptor (D2R) density in the striatum. At the transcriptional level, the D2R mRNA was also enhanced in the striatum. Quantitative in situ hybridization studies revealed that the number of neurons expressing the D2R mRNA was significantly enhanced in treated rats, whereas the mean amount of message per cell was unchanged. These changes could represent the neurobiological substrate of the observed sensitization. These results suggest that the D2R gene is under glutamate control via NMDA receptor in striatal neurons.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lannes</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institut de Physiologie, Faculté de Médecine, Strasbourg, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Micheletti</LastName><ForeName>G</ForeName><Initials>G</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>Neurosci Biobehav Rev</MedlineTA><NlmUniqueID>7806090</NlmUniqueID><ISSNLinking>0149-7634</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018691">Excitatory Amino Acid Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017448">Receptors, Dopamine D2</NameOfSubstance></Chemical><Chemical><RegistryNumber>6LR8C1B66Q</RegistryNumber><NameOfSubstance UI="D016291">Dizocilpine Maleate</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015152" MajorTopicYN="N">Blotting, Northern</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016291" MajorTopicYN="N">Dizocilpine Maleate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018691" MajorTopicYN="N">Excitatory Amino Acid Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017403" MajorTopicYN="N">In Situ Hybridization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017072" MajorTopicYN="N">Neostriatum</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017448" MajorTopicYN="N">Receptors, Dopamine D2</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9195599</ArticleId><ArticleId IdType="pii">S0149-7634(96)00041-3</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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