Differences between rat primary cortical neurons and astrocytes in purine release evoked by ischemic conditions.
Identifieur interne : 002F79 ( Main/Exploration ); précédent : 002F78; suivant : 002F80Differences between rat primary cortical neurons and astrocytes in purine release evoked by ischemic conditions.
Auteurs : F E Parkinson [Canada] ; C J D. Sinclair ; T. Othman ; N J Haughey ; J D GeigerSource :
- Neuropharmacology [ 0028-3908 ] ; 2002.
English descriptors
- KwdEn :
- Adenine Nucleotides (metabolism), Adenosine Deaminase Inhibitors, Adenosine Kinase (antagonists & inhibitors), Adenosine Triphosphate (physiology), Animals, Antimetabolites (pharmacology), Astrocytes (drug effects), Astrocytes (metabolism), Brain Ischemia (metabolism), Cells, Cultured, Cerebral Cortex (cytology), Cerebral Cortex (drug effects), Cerebral Cortex (metabolism), Chromatography, Thin Layer, Enzyme Inhibitors (pharmacology), Extracellular Space (drug effects), Extracellular Space (metabolism), Glucose (physiology), Hypoxanthine (metabolism), Hypoxia-Ischemia, Brain (metabolism), Inosine (metabolism), Iodoacetates (pharmacology), Neurons (drug effects), Neurons (metabolism), Purines (metabolism), Rats, Sodium Cyanide (pharmacology).
- MESH :
- chemical , antagonists & inhibitors : Adenosine Kinase.
- chemical , metabolism : Adenine Nucleotides, Hypoxanthine, Inosine, Purines.
- chemical , pharmacology : Antimetabolites, Enzyme Inhibitors, Iodoacetates, Sodium Cyanide.
- chemical , physiology : Adenosine Triphosphate, Glucose.
- chemical : Adenosine Deaminase Inhibitors.
- cytology : Cerebral Cortex.
- drug effects : Astrocytes, Cerebral Cortex, Extracellular Space, Neurons.
- metabolism : Astrocytes, Brain Ischemia, Cerebral Cortex, Extracellular Space, Hypoxia-Ischemia, Brain, Neurons.
- Animals, Cells, Cultured, Chromatography, Thin Layer, Rats.
Abstract
In the brain, the levels of adenosine increase up to 100-fold during cerebral ischernia; however, the roles of specific cell types, enzymatic pathways and membrane transport processes in regulating intra- and extracellular concentrations of adenosine are poorly characterized. Rat primary cortical neurons and astrocytes were incubated with [(3)H]adenine for 30 min to radiolabel intracellular ATP. Cells were then treated with buffer, glucose deprivation (GD), oxygen-glucose deprivation (OGD), 100 micro M sodium cyanide (NaCN) or 500 micro M iodoacetate (IAA) for 1 h to stimulate the metabolism of ATP and cellular release of [(3)H]purines. The nucleoside transport inhibitor dipyridamole (DPR) (10 micro M), the adenosine kinase inhibitor iodotubercidin (ITU) (1 micro M), the adenosine deaminase inhibitor EHNA (1 micro M) and the purine nucleoside phosphorylase inhibitor BCX-34 (10 micro M) were tested to investigate the contribution of specific enzymes and transporters in the metabolism and release of purines from each cell type. Our results indicate that (a). under basal conditions astrocytes released significantly more [(3)H]adenine nucleotides and [(3)H]adenosine than neurons, (b). OGD, NaCN and IAA conditions produced significant increases in [(3)H]adenosine release from neurons but not astrocytes, and (c) DPR blocked [(3)H]inosine release from both astrocytes and neurons but only blocked [(3)H]adenosine release from neurons. These data suggest that, in these experimental conditions, adenosine was formed by an intracellular pathway in neurons and then released via a nucleoside transporter. In contrast, adenine nucleotide release and extracellular metabolism to adenosine appeared to predominate in astrocytes.
PubMed: 12384169
Affiliations:
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Othman</name></author><author><name sortKey="Haughey, N J" sort="Haughey, N J" uniqKey="Haughey N" first="N J" last="Haughey">N J Haughey</name></author><author><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12384169</idno><idno type="pmid">12384169</idno><idno type="wicri:Area/PubMed/Corpus">001487</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001487</idno><idno type="wicri:Area/PubMed/Curation">001487</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001487</idno><idno type="wicri:Area/PubMed/Checkpoint">001487</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001487</idno><idno type="wicri:Area/Ncbi/Merge">000252</idno><idno type="wicri:Area/Ncbi/Curation">000252</idno><idno type="wicri:Area/Ncbi/Checkpoint">000252</idno><idno type="wicri:doubleKey">0028-3908:2002:Parkinson F:differences:between:rat</idno><idno type="wicri:Area/Main/Merge">003413</idno><idno type="wicri:Area/Main/Curation">002F79</idno><idno type="wicri:Area/Main/Exploration">002F79</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differences between rat primary cortical neurons and astrocytes in purine release evoked by ischemic conditions.</title><author><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, 753 McDermot Avenue, Winnipeg, MB, R3E 0T6 Canada. Fiona_Parkinson@umanitoba.ca</nlm:affiliation><country wicri:rule="url">Canada</country></affiliation></author><author><name sortKey="Sinclair, C J D" sort="Sinclair, C J D" uniqKey="Sinclair C" first="C J D" last="Sinclair">C J D. Sinclair</name></author><author><name sortKey="Othman, T" sort="Othman, T" uniqKey="Othman T" first="T" last="Othman">T. Othman</name></author><author><name sortKey="Haughey, N J" sort="Haughey, N J" uniqKey="Haughey N" first="N J" last="Haughey">N J Haughey</name></author><author><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name></author></analytic><series><title level="j">Neuropharmacology</title><idno type="ISSN">0028-3908</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine Nucleotides (metabolism)</term><term>Adenosine Deaminase Inhibitors</term><term>Adenosine Kinase (antagonists & inhibitors)</term><term>Adenosine Triphosphate (physiology)</term><term>Animals</term><term>Antimetabolites (pharmacology)</term><term>Astrocytes (drug effects)</term><term>Astrocytes (metabolism)</term><term>Brain Ischemia (metabolism)</term><term>Cells, Cultured</term><term>Cerebral Cortex (cytology)</term><term>Cerebral Cortex (drug effects)</term><term>Cerebral Cortex (metabolism)</term><term>Chromatography, Thin Layer</term><term>Enzyme Inhibitors (pharmacology)</term><term>Extracellular Space (drug effects)</term><term>Extracellular Space (metabolism)</term><term>Glucose (physiology)</term><term>Hypoxanthine (metabolism)</term><term>Hypoxia-Ischemia, Brain (metabolism)</term><term>Inosine (metabolism)</term><term>Iodoacetates (pharmacology)</term><term>Neurons (drug effects)</term><term>Neurons (metabolism)</term><term>Purines (metabolism)</term><term>Rats</term><term>Sodium Cyanide (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Adenosine Kinase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenine Nucleotides</term><term>Hypoxanthine</term><term>Inosine</term><term>Purines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antimetabolites</term><term>Enzyme Inhibitors</term><term>Iodoacetates</term><term>Sodium Cyanide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Adenosine Triphosphate</term><term>Glucose</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Adenosine Deaminase Inhibitors</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Astrocytes</term><term>Cerebral Cortex</term><term>Extracellular Space</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Brain Ischemia</term><term>Cerebral Cortex</term><term>Extracellular Space</term><term>Hypoxia-Ischemia, Brain</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Chromatography, Thin Layer</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the brain, the levels of adenosine increase up to 100-fold during cerebral ischernia; however, the roles of specific cell types, enzymatic pathways and membrane transport processes in regulating intra- and extracellular concentrations of adenosine are poorly characterized. Rat primary cortical neurons and astrocytes were incubated with [(3)H]adenine for 30 min to radiolabel intracellular ATP. Cells were then treated with buffer, glucose deprivation (GD), oxygen-glucose deprivation (OGD), 100 micro M sodium cyanide (NaCN) or 500 micro M iodoacetate (IAA) for 1 h to stimulate the metabolism of ATP and cellular release of [(3)H]purines. The nucleoside transport inhibitor dipyridamole (DPR) (10 micro M), the adenosine kinase inhibitor iodotubercidin (ITU) (1 micro M), the adenosine deaminase inhibitor EHNA (1 micro M) and the purine nucleoside phosphorylase inhibitor BCX-34 (10 micro M) were tested to investigate the contribution of specific enzymes and transporters in the metabolism and release of purines from each cell type. Our results indicate that (a). under basal conditions astrocytes released significantly more [(3)H]adenine nucleotides and [(3)H]adenosine than neurons, (b). OGD, NaCN and IAA conditions produced significant increases in [(3)H]adenosine release from neurons but not astrocytes, and (c) DPR blocked [(3)H]inosine release from both astrocytes and neurons but only blocked [(3)H]adenosine release from neurons. These data suggest that, in these experimental conditions, adenosine was formed by an intracellular pathway in neurons and then released via a nucleoside transporter. In contrast, adenine nucleotide release and extracellular metabolism to adenosine appeared to predominate in astrocytes.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name><name sortKey="Haughey, N J" sort="Haughey, N J" uniqKey="Haughey N" first="N J" last="Haughey">N J Haughey</name><name sortKey="Othman, T" sort="Othman, T" uniqKey="Othman T" first="T" last="Othman">T. Othman</name><name sortKey="Sinclair, C J D" sort="Sinclair, C J D" uniqKey="Sinclair C" first="C J D" last="Sinclair">C J D. Sinclair</name></noCountry><country name="Canada"><noRegion><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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