Modulation of adenosine release from rat spinal cord by adenosine deaminase and adenosine kinase inhibitors

Krystyna Golembiowska; Thomas D. White; Jana Sawynok

doi:10.1016/0006-8993(95)00926-H

Modulation of adenosine release from rat spinal cord by adenosine deaminase and adenosine kinase inhibitors

Krystyna Golembiowska, Thomas D. White, Jana Sawynok

Medicine

Research output: Contribution to journal › Article › peer-review

26 Citations (Scopus)

Abstract

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′-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.

Original language	English
Pages (from-to)	315-320
Number of pages	6
Journal	Brain Research
Volume	699
Issue number	2
DOIs	https://doi.org/10.1016/0006-8993(95)00926-H
Publication status	Published - Nov 20 1995

Bibliographical note

Funding Information:
This work was supported by the Medical Research Council of Canada. We thank Parke Davies Pharmaceuticals for the provision of 2'-deoxycoformycin.

ASJC Scopus Subject Areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

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10.1016/0006-8993(95)00926-H

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title = "Modulation of adenosine release from rat spinal cord by adenosine deaminase and adenosine kinase inhibitors",

abstract = "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′-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.",

author = "Krystyna Golembiowska and White, {Thomas D.} and Jana Sawynok",

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AU - Golembiowska, Krystyna

AU - White, Thomas D.

AU - Sawynok, Jana

N1 - Funding Information: This work was supported by the Medical Research Council of Canada. We thank Parke Davies Pharmaceuticals for the provision of 2'-deoxycoformycin.

PY - 1995/11/20

Y1 - 1995/11/20

N2 - 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′-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.

AB - 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′-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.

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Modulation of adenosine release from rat spinal cord by adenosine deaminase and adenosine kinase inhibitors

Abstract

Bibliographical note

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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