Modulation of adenosine release from rat spinal cord by adenosine deaminase and adenosine kinase inhibitors
| Autor: | Thomas D. White, Jana Sawynok, Krystyna Golembiowska |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Adenosine Time Factors Adenosine Deaminase Adenosine kinase Rats Sprague-Dawley Adenosine A1 receptor Internal medicine medicine Animals Molecular Biology Dose-Response Relationship Drug Morphine biology Chemistry General Neuroscience Purinergic signalling Adenosine A3 receptor Adenosine receptor Rats Endocrinology Spinal Cord biology.protein Neurology (clinical) Adenosine Deaminase Inhibitor Pentostatin Adenosine A2B receptor Developmental Biology medicine.drug |
| Zdroj: | Brain Research. 699:315-320 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/0006-8993(95)00926-h |
| Popis: | Adenosine, a modulator of pain processing in the spinal cord, is metabolized by adenosine kinase and adenosine deaminase. In this study we determined which of these mechanisms is more important for the regulation of endogenous adenosine levels in the rat spinal cord. The effects of the adenosine kinase inhibitors, 5'-amino-5'-deoxyadenosine (NH2dAD) and iodotubercidin (IOT), and the adenosine deaminase inhibitor, 2'-deoxycoformycin (DCF), on adenosine release in a spinal cord superfusion model were studied. DCF markedly increased basal adenosine levels detected in perfusates and was more potent than NH2dAD and IOT in this regard. Coadministration of DCF with NH2dAD produced an enhanced effect compared to the inhibitors alone. NH2dAD, but not DCF, potentiated morphine-evoked adenosine release. These results suggest that adenosine deaminase may be the predominant pathway for adenosine metabolism in this experimental model. |
| Databáze: | OpenAIRE |
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