Purine metabolite inosine is an adrenergic neurotrophic substance for cultured chicken sympathetic neurons

Details

Serval ID
serval:BIB_54C8F96934D1
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Purine metabolite inosine is an adrenergic neurotrophic substance for cultured chicken sympathetic neurons
Journal
Proceedings of the National Academy of Sciences of the United States of America
Author(s)
Zurn  A. D., Do  K. Q.
ISSN
0027-8424 (Print)
Publication state
Published
Issued date
11/1988
Volume
85
Number
21
Pages
8301-5
Notes
Journal Article Research Support, Non-U.S. Gov't --- Old month value: Nov
Abstract
Purines are ubiquitous endogenous cellular metabolites that have been postulated as neurotransmitters or neuromodulators in the nervous system. Recently, we showed that a low-molecular-mass component present in liver-conditioned medium selectively enhances the adrenergic properties of dissociated chicken sympathetic neurons in culture. We report here that this substance is inosine, a purine metabolite. Indeed, analysis of the low-molecular-mass fraction of liver-conditioned medium by HPLC shows that the neurotrophic activity coelutes with and has the same absorption spectrum as inosine. Inosine increases incorporation of [3H]leucine into neuronal protein and stimulates catecholamine, but not acetylcholine, production by the sympathetic neurons in a dose-dependent fashion (half-maximal stimulation at 10(-6) M). This effect can be blocked by 5 x 10(-6) M dipyridamole, an inhibitor of nucleoside transport. Inosine therefore appears to be capable of modulating adrenergic phenotypic expression in cultured sympathetic neurons by acting via an as-yet-unknown intracellular pathway.
Keywords
Animals Cells, Cultured Chick Embryo Chromatography, High Pressure Liquid Dipyridamole/pharmacology Dose-Response Relationship, Drug Inosine/*metabolism Leucine/metabolism Neurons/*metabolism Sympathetic Nervous System/*cytology/metabolism Theophylline/pharmacology
Pubmed
Web of science
Open Access
Yes
Create date
28/01/2008 9:44
Last modification date
20/08/2019 15:09
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