Involvement of bidirectional adenosine transporters in the release of L-[3H]adenosine from rat brain synaptosomal preparations.
Identifieur interne : 003F16 ( Main/Exploration ); précédent : 003F15; suivant : 003F17Involvement of bidirectional adenosine transporters in the release of L-[3H]adenosine from rat brain synaptosomal preparations.
Auteurs : J G Gu [Canada] ; I O Foga ; F E Parkinson ; J D GeigerSource :
- Journal of neurochemistry [ 0022-3042 ] ; 1995.
English descriptors
- KwdEn :
- Adenosine (secretion), Animals, Biological Transport (drug effects), Brain (secretion), Carrier Proteins (metabolism), Dilazep (pharmacology), Dipyridamole (pharmacology), Kinetics, Male, Membrane Proteins (metabolism), Nucleoside Transport Proteins, Potassium Chloride (pharmacology), Rats, Rats, Sprague-Dawley, Synaptosomes (secretion), Thioinosine (analogs & derivatives), Thioinosine (pharmacology), Tritium.
- MESH :
- chemical , analogs & derivatives : Thioinosine.
- chemical , metabolism : Carrier Proteins, Membrane Proteins.
- chemical , pharmacology : Dilazep, Dipyridamole, Potassium Chloride, Thioinosine.
- chemical , secretion : Adenosine.
- drug effects : Biological Transport.
- secretion : Brain, Synaptosomes.
- Animals, Kinetics, Male, Nucleoside Transport Proteins, Rats, Rats, Sprague-Dawley, Tritium.
Abstract
Adenosine transport inhibitors as enhancers of extracellular levels of endogenous adenosine would, presumably, only be effective if, for example, (1) the inhibitors block influx to a greater degree than efflux (release) of intracellular adenosine or (2) the inhibitors block equally well the influx and efflux of adenosine, but significant amounts of adenosine are formed as a result of dephosphorylation of released adenine nucleotides. Limited information is available regarding the directional symmetry of adenosine transporters in neural cells. Using rat brain crude P2 synaptosomal preparations preloaded with L-[3H]adenosine, our objectives here were to determine (1) if L-[3H]adenosine, a substrate for adenosine transporters that is more metabolically stable than physiological D-adenosine, was being released from synaptosomal preparations, (2) the optimal conditions necessary to observe the release, and (3) the degree to which this release was mediated by efflux through bidirectional nucleoside transporters. L-[3H]Adenosine release was found to be concentration and time dependent, temperature sensitive, and linear with synaptosomal protein. L-[3H]Adenosine release was inhibited dose-dependently by dipyridamole, nitrobenzylthioinosine, and dilazep; at concentrations of 100 microM inhibition was at least 40% for dipyridamole, 52% for nitrobenzylthioinosine, and 49% for dilazep. After loading with L-[3H]adenosine alone or I-[3H]adenosine plus unlabeled L-adenosine, D-adenosine, or uridine, L-[3H]adenosine release was inhibited 42% by L-adenosine, 69% by uridine, and 81% by D-adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed: 7722493
Affiliations:
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sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</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="1995">1995</date><idno type="RBID">pubmed:7722493</idno><idno type="pmid">7722493</idno><idno type="wicri:Area/PubMed/Corpus">001921</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001921</idno><idno type="wicri:Area/PubMed/Curation">001921</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001921</idno><idno type="wicri:Area/PubMed/Checkpoint">001921</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001921</idno><idno type="wicri:Area/Ncbi/Merge">002406</idno><idno type="wicri:Area/Ncbi/Curation">002406</idno><idno type="wicri:Area/Ncbi/Checkpoint">002406</idno><idno 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type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Foga, I O" sort="Foga, I O" uniqKey="Foga I" first="I O" last="Foga">I O Foga</name></author><author><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</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">Journal of neurochemistry</title><idno type="ISSN">0022-3042</idno><imprint><date when="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine (secretion)</term><term>Animals</term><term>Biological Transport (drug effects)</term><term>Brain (secretion)</term><term>Carrier Proteins (metabolism)</term><term>Dilazep (pharmacology)</term><term>Dipyridamole (pharmacology)</term><term>Kinetics</term><term>Male</term><term>Membrane Proteins (metabolism)</term><term>Nucleoside Transport Proteins</term><term>Potassium Chloride (pharmacology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Synaptosomes (secretion)</term><term>Thioinosine (analogs & derivatives)</term><term>Thioinosine (pharmacology)</term><term>Tritium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Thioinosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Membrane Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dilazep</term><term>Dipyridamole</term><term>Potassium Chloride</term><term>Thioinosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Adenosine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Biological Transport</term></keywords><keywords scheme="MESH" qualifier="secretion" xml:lang="en"><term>Brain</term><term>Synaptosomes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Kinetics</term><term>Male</term><term>Nucleoside Transport Proteins</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Tritium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine transport inhibitors as enhancers of extracellular levels of endogenous adenosine would, presumably, only be effective if, for example, (1) the inhibitors block influx to a greater degree than efflux (release) of intracellular adenosine or (2) the inhibitors block equally well the influx and efflux of adenosine, but significant amounts of adenosine are formed as a result of dephosphorylation of released adenine nucleotides. Limited information is available regarding the directional symmetry of adenosine transporters in neural cells. Using rat brain crude P2 synaptosomal preparations preloaded with L-[3H]adenosine, our objectives here were to determine (1) if L-[3H]adenosine, a substrate for adenosine transporters that is more metabolically stable than physiological D-adenosine, was being released from synaptosomal preparations, (2) the optimal conditions necessary to observe the release, and (3) the degree to which this release was mediated by efflux through bidirectional nucleoside transporters. L-[3H]Adenosine release was found to be concentration and time dependent, temperature sensitive, and linear with synaptosomal protein. L-[3H]Adenosine release was inhibited dose-dependently by dipyridamole, nitrobenzylthioinosine, and dilazep; at concentrations of 100 microM inhibition was at least 40% for dipyridamole, 52% for nitrobenzylthioinosine, and 49% for dilazep. After loading with L-[3H]adenosine alone or I-[3H]adenosine plus unlabeled L-adenosine, D-adenosine, or uridine, L-[3H]adenosine release was inhibited 42% by L-adenosine, 69% by uridine, and 81% by D-adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Manitoba</li></region><settlement><li>Winnipeg</li></settlement><orgName><li>Université du Manitoba</li></orgName></list><tree><noCountry><name sortKey="Foga, I O" sort="Foga, I O" uniqKey="Foga I" first="I O" last="Foga">I O Foga</name><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name></noCountry><country name="Canada"><region name="Manitoba"><name sortKey="Gu, J G" sort="Gu, J G" uniqKey="Gu J" first="J G" last="Gu">J G Gu</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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