Abstract
The role of adenosine receptor agonists in the convulsant activity of mitochondrial toxin, 3-nitropropionic acid (3-NPA), was studied in mice. The occurrence of seizures evoked by peripheral application of 3-NPA was inhibited with the use of A1 adenosine receptor agonist, R-N6-phenylisopropyladenosine and A1/A2 agonist, 2-chloroadenosine. Moreover, both drugs prevented 3-NPA-induced mortality. Similarly, A1/A2 agonist, 5'-N-ethylcarboxamidoadenosine, protected against seizures evoked by the intracerebral administration of 3-NPA, and this effect was reversed by the co-application of adenosine receptor antagonist, 8-(p-sulfophenyl)theophylline. Obtained results suggest that A1 adenosine receptor activation may modulate the chain of events leading to the development of 3-NPA-induced seizures.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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2-Chloroadenosine / pharmacology
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Adenosine-5'-(N-ethylcarboxamide) / pharmacology
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Animals
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Convulsants
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Epilepsy / chemically induced*
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Epilepsy / prevention & control*
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Hormone Antagonists / pharmacology
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Male
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Mice
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Mitochondria / drug effects
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Neuroprotective Agents / pharmacology*
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Nitro Compounds
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Phenylisopropyladenosine / pharmacology
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Propionates* / pharmacology
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Purinergic P1 Receptor Agonists*
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Purinergic P1 Receptor Antagonists
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Theophylline / analogs & derivatives*
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Theophylline / pharmacology
Substances
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Convulsants
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Hormone Antagonists
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Neuroprotective Agents
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Nitro Compounds
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Propionates
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Purinergic P1 Receptor Agonists
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Purinergic P1 Receptor Antagonists
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2-Chloroadenosine
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Phenylisopropyladenosine
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Adenosine-5'-(N-ethylcarboxamide)
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8-(4-sulfophenyl)theophylline
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Theophylline
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3-nitropropionic acid