Co-administration of adenosine kinase and deaminase inhibitors produces supra-additive potentiation of N -methyl-d-aspartate-evoked adenosine formation in cortex
Identifieur interne : 003914 ( Main/Exploration ); précédent : 003913; suivant : 003915Co-administration of adenosine kinase and deaminase inhibitors produces supra-additive potentiation of N -methyl-d-aspartate-evoked adenosine formation in cortex
Auteurs : Matthew O. Hebb [Canada] ; Thomas D. White [Canada]Source :
- European Journal of Pharmacology [ 0014-2999 ] ; 1998.
Abstract
Activation of glutamate receptors triggers the release of adenosine, which exerts important inhibitory actions in the brain. Evoked adenosine release is potentiated when either adenosine kinase or adenosine deaminase are inhibited. We studied the effects of concurrent inhibition of adenosine kinase and adenosine deaminase on N-methyl-d-aspartate (NMDA)-evoked formation of extracellular adenosine in slices of rat parietal cortex, to determine if combinations of inhibitors of adenosine kinase and adenosine deaminase can produce supra-additive potentiation of this adenosine formation. Combinations of low concentrations of the adenosine kinase inhibitors 5′-amino-5′-deoxyadenosine (0.2 μM) or 5′-iodotubercidin (0.01 μM) with a low concentration of the adenosine deaminase inhibitor 2′-deoxycoformycin (0.2 μM) produced additive potentiations of NMDA-evoked adenosine release from slices of rat parietal cortex. However, combinations of low concentrations of 5′-amino-5′-deoxyadenosine (0.2 μM) or 5′-iodotubercidin (0.01 μM) with a maximal concentration of 2′-deoxycoformycin (200 μM) produced supra-additive potentiation of NMDA-evoked adenosine release. These findings suggest that such combinations of adenosine kinase inhibitors with adenosine deaminase inhibitors may provide useful strategies for developing therapies to treat disorders associated with excessive NMDA receptor activation, such as seizures, ischemic damage and neurodegenerative diseases.
Url:
DOI: 10.1016/S0014-2999(97)01582-3
Affiliations:
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Hebb</name><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Department of Pharmacology, Dalhousie University, Halifax, NS</wicri:regionArea><wicri:noRegion>NS</wicri:noRegion></affiliation></author><author><name sortKey="White, Thomas D" sort="White, Thomas D" uniqKey="White T" first="Thomas D" last="White">Thomas D. White</name><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Department of Pharmacology, Dalhousie University, Halifax, NS</wicri:regionArea><wicri:noRegion>NS</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Pharmacology</title><title level="j" type="abbrev">EJP</title><idno type="ISSN">0014-2999</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">344</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="121">121</biblScope><biblScope unit="page" to="125">125</biblScope></imprint><idno type="ISSN">0014-2999</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2999</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activation of glutamate receptors triggers the release of adenosine, which exerts important inhibitory actions in the brain. Evoked adenosine release is potentiated when either adenosine kinase or adenosine deaminase are inhibited. We studied the effects of concurrent inhibition of adenosine kinase and adenosine deaminase on N-methyl-d-aspartate (NMDA)-evoked formation of extracellular adenosine in slices of rat parietal cortex, to determine if combinations of inhibitors of adenosine kinase and adenosine deaminase can produce supra-additive potentiation of this adenosine formation. Combinations of low concentrations of the adenosine kinase inhibitors 5′-amino-5′-deoxyadenosine (0.2 μM) or 5′-iodotubercidin (0.01 μM) with a low concentration of the adenosine deaminase inhibitor 2′-deoxycoformycin (0.2 μM) produced additive potentiations of NMDA-evoked adenosine release from slices of rat parietal cortex. However, combinations of low concentrations of 5′-amino-5′-deoxyadenosine (0.2 μM) or 5′-iodotubercidin (0.01 μM) with a maximal concentration of 2′-deoxycoformycin (200 μM) produced supra-additive potentiation of NMDA-evoked adenosine release. These findings suggest that such combinations of adenosine kinase inhibitors with adenosine deaminase inhibitors may provide useful strategies for developing therapies to treat disorders associated with excessive NMDA receptor activation, such as seizures, ischemic damage and neurodegenerative diseases.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Hebb, Matthew O" sort="Hebb, Matthew O" uniqKey="Hebb M" first="Matthew O" last="Hebb">Matthew O. Hebb</name></noRegion><name sortKey="White, Thomas D" sort="White, Thomas D" uniqKey="White T" first="Thomas D" last="White">Thomas D. 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