Astrocytes affect the profile of purines released from cultured cortical neurons.
Identifieur interne : 000F55 ( PubMed/Corpus ); précédent : 000F54; suivant : 000F56Astrocytes affect the profile of purines released from cultured cortical neurons.
Auteurs : Christina R. Zamzow ; Wei Xiong ; Fiona E. ParkinsonSource :
- Journal of neuroscience research [ 1097-4547 ] ; 2008.
English descriptors
- KwdEn :
- Animals, Astrocytes (cytology), Astrocytes (drug effects), Astrocytes (secretion), Cells, Cultured, Cerebral Cortex (cytology), Cerebral Cortex (drug effects), Cerebral Cortex (secretion), Coculture Techniques, N-Methylaspartate (pharmacology), Neurons (cytology), Neurons (drug effects), Neurons (secretion), Purines (agonists), Purines (metabolism), Rats, Rats, Sprague-Dawley, Signal Transduction (drug effects), Signal Transduction (physiology).
- MESH :
- chemical , agonists : Purines.
- chemical , metabolism : Purines.
- chemical , pharmacology : N-Methylaspartate.
- cytology : Astrocytes, Cerebral Cortex, Neurons.
- drug effects : Astrocytes, Cerebral Cortex, Neurons, Signal Transduction.
- physiology : Signal Transduction.
- secretion : Astrocytes, Cerebral Cortex, Neurons.
- Animals, Cells, Cultured, Coculture Techniques, Rats, Rats, Sprague-Dawley.
Abstract
Adenosine (ADO) is produced by cultured neurons and astrocytes, albeit by different pathways, during in vitro stroke models (Parkinson and Xiong [2004] J. Neurochem. 88:1305-1312). Expression of ecto-5' nucleotidase (e-N), the enzyme responsible for extracellular dephosphorylation of AMP to ADO, is more abundant in astrocytes than neurons. Therefore, we tested the hypothesis that N-methyl-D-aspartate (NMDA) evokes ADO release per se from neurons, whereas dephosphorylation of extracellular adenine nucleotides contributes to NMDA-evoked ADO production in the presence of astrocytes. We used four different cell preparations-cortical rat neurons, cortical rat astrocytes, cocultures of neurons and astrocytes, and transient cocultures of neurons with astrocytes on transwell filters-to show that astrocytes contribute to NMDA-evoked increases in extracellular ADO. NMDA significantly increased ADO and inosine (INO) production from cultured cortical neurons but only increased extracellular INO production from cocultures. In neurons, the equilibrative nucleoside transport (ENT) inhibitor dipyridamole (DPR) prevented NMDA-evoked ADO and INO production, whereas the e-N inhibitor alpha,beta-methylene ADP (AOPCP) had no effect. Conversely, from both cocultures and transient cocultures DPR significantly decreased NMDA-evoked INO but not ADO generation. AOPCP inhibited NMDA-evoked production of both ADO and INO from transient cocultures. In the absence of astrocytes, NMDA evoked release of intracellular ADO and INO from cultured cortical neurons through ENT. However, in the presence of astrocytes, extracellular conversion of adenine nucleotides to ADO contributed significantly to NMDA-evoked production of this purine.
DOI: 10.1002/jnr.21718
PubMed: 18478552
Links to Exploration step
pubmed:18478552Le document en format XML
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Parkinson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18478552</idno><idno type="pmid">18478552</idno><idno type="doi">10.1002/jnr.21718</idno><idno type="wicri:Area/PubMed/Corpus">000F55</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F55</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Astrocytes affect the profile of purines released from cultured cortical neurons.</title><author><name sortKey="Zamzow, Christina R" sort="Zamzow, Christina R" uniqKey="Zamzow C" first="Christina R" last="Zamzow">Christina R. Zamzow</name><affiliation><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Xiong, Wei" sort="Xiong, Wei" uniqKey="Xiong W" first="Wei" last="Xiong">Wei Xiong</name></author><author><name sortKey="Parkinson, Fiona E" sort="Parkinson, Fiona E" uniqKey="Parkinson F" first="Fiona E" last="Parkinson">Fiona E. Parkinson</name></author></analytic><series><title level="j">Journal of neuroscience research</title><idno type="eISSN">1097-4547</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Astrocytes (cytology)</term><term>Astrocytes (drug effects)</term><term>Astrocytes (secretion)</term><term>Cells, Cultured</term><term>Cerebral Cortex (cytology)</term><term>Cerebral Cortex (drug effects)</term><term>Cerebral Cortex (secretion)</term><term>Coculture Techniques</term><term>N-Methylaspartate (pharmacology)</term><term>Neurons (cytology)</term><term>Neurons (drug effects)</term><term>Neurons (secretion)</term><term>Purines (agonists)</term><term>Purines (metabolism)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Signal Transduction (drug effects)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Purines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Purines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>N-Methylaspartate</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Astrocytes</term><term>Cerebral Cortex</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Astrocytes</term><term>Cerebral Cortex</term><term>Neurons</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="secretion" xml:lang="en"><term>Astrocytes</term><term>Cerebral Cortex</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Coculture Techniques</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine (ADO) is produced by cultured neurons and astrocytes, albeit by different pathways, during in vitro stroke models (Parkinson and Xiong [2004] J. Neurochem. 88:1305-1312). Expression of ecto-5' nucleotidase (e-N), the enzyme responsible for extracellular dephosphorylation of AMP to ADO, is more abundant in astrocytes than neurons. Therefore, we tested the hypothesis that N-methyl-D-aspartate (NMDA) evokes ADO release per se from neurons, whereas dephosphorylation of extracellular adenine nucleotides contributes to NMDA-evoked ADO production in the presence of astrocytes. We used four different cell preparations-cortical rat neurons, cortical rat astrocytes, cocultures of neurons and astrocytes, and transient cocultures of neurons with astrocytes on transwell filters-to show that astrocytes contribute to NMDA-evoked increases in extracellular ADO. NMDA significantly increased ADO and inosine (INO) production from cultured cortical neurons but only increased extracellular INO production from cocultures. In neurons, the equilibrative nucleoside transport (ENT) inhibitor dipyridamole (DPR) prevented NMDA-evoked ADO and INO production, whereas the e-N inhibitor alpha,beta-methylene ADP (AOPCP) had no effect. Conversely, from both cocultures and transient cocultures DPR significantly decreased NMDA-evoked INO but not ADO generation. AOPCP inhibited NMDA-evoked production of both ADO and INO from transient cocultures. In the absence of astrocytes, NMDA evoked release of intracellular ADO and INO from cultured cortical neurons through ENT. However, in the presence of astrocytes, extracellular conversion of adenine nucleotides to ADO contributed significantly to NMDA-evoked production of this purine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18478552</PMID><DateCreated><Year>2008</Year><Month>08</Month><Day>22</Day></DateCreated><DateCompleted><Year>2009</Year><Month>03</Month><Day>16</Day></DateCompleted><DateRevised><Year>2008</Year><Month>08</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1097-4547</ISSN><JournalIssue CitedMedium="Internet"><Volume>86</Volume><Issue>12</Issue><PubDate><Year>2008</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Journal of neuroscience research</Title><ISOAbbreviation>J. Neurosci. Res.</ISOAbbreviation></Journal><ArticleTitle>Astrocytes affect the profile of purines released from cultured cortical neurons.</ArticleTitle><Pagination><MedlinePgn>2641-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/jnr.21718</ELocationID><Abstract><AbstractText>Adenosine (ADO) is produced by cultured neurons and astrocytes, albeit by different pathways, during in vitro stroke models (Parkinson and Xiong [2004] J. Neurochem. 88:1305-1312). Expression of ecto-5' nucleotidase (e-N), the enzyme responsible for extracellular dephosphorylation of AMP to ADO, is more abundant in astrocytes than neurons. Therefore, we tested the hypothesis that N-methyl-D-aspartate (NMDA) evokes ADO release per se from neurons, whereas dephosphorylation of extracellular adenine nucleotides contributes to NMDA-evoked ADO production in the presence of astrocytes. We used four different cell preparations-cortical rat neurons, cortical rat astrocytes, cocultures of neurons and astrocytes, and transient cocultures of neurons with astrocytes on transwell filters-to show that astrocytes contribute to NMDA-evoked increases in extracellular ADO. NMDA significantly increased ADO and inosine (INO) production from cultured cortical neurons but only increased extracellular INO production from cocultures. In neurons, the equilibrative nucleoside transport (ENT) inhibitor dipyridamole (DPR) prevented NMDA-evoked ADO and INO production, whereas the e-N inhibitor alpha,beta-methylene ADP (AOPCP) had no effect. Conversely, from both cocultures and transient cocultures DPR significantly decreased NMDA-evoked INO but not ADO generation. AOPCP inhibited NMDA-evoked production of both ADO and INO from transient cocultures. In the absence of astrocytes, NMDA evoked release of intracellular ADO and INO from cultured cortical neurons through ENT. However, in the presence of astrocytes, extracellular conversion of adenine nucleotides to ADO contributed significantly to NMDA-evoked production of this purine.</AbstractText><CopyrightInformation>(c) 2008 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zamzow</LastName><ForeName>Christina R</ForeName><Initials>CR</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiong</LastName><ForeName>Wei</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Parkinson</LastName><ForeName>Fiona E</ForeName><Initials>FE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><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>J Neurosci Res</MedlineTA><NlmUniqueID>7600111</NlmUniqueID><ISSNLinking>0360-4012</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011687">Purines</NameOfSubstance></Chemical><Chemical><RegistryNumber>6384-92-5</RegistryNumber><NameOfSubstance UI="D016202">N-Methylaspartate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001253" MajorTopicYN="N">Astrocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000557" MajorTopicYN="Y">secretion</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000557" MajorTopicYN="Y">secretion</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018920" MajorTopicYN="N">Coculture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016202" MajorTopicYN="N">N-Methylaspartate</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000557" MajorTopicYN="Y">secretion</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011687" MajorTopicYN="N">Purines</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>5</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>3</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>5</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18478552</ArticleId><ArticleId IdType="doi">10.1002/jnr.21718</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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