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Published July 1985 | Published
Journal Article Open

Potassium-stimulated Purine Release by Cultured Sympathetic Neurons

Abstract

Environmental factors can influence cultured sympathetic neurons to acquire several different neurotransmitter phenotypes. Cholinergic and noradrenergic transmitter status can be influenced by heart cell conditioned medium, chronic depolarization (Patterson, P. H. (1978) Annu. Rev. Neurosci. 1:1–17), and rat serum (Wolinsky, E. J., and P. H. Patterson, (1985) J. Neurosci. 5:1509–1512); formation of electrical synapses can be induced by insulin (Wolinsky, E. J., H. Patterson, and A. L. Willard (1985) J. Neurosci., 5:1675–1679). Purine release has also been proposed as a possible transmission mode for sympathetic neurons (Potter, D. D., E. J. Furshpan, and S. C. Landis (1983) Fred. Proc. 42:1626–1632), and as such, it is another candidate for environmental modulation. In this report, we assess the ability of sympathetic neuron cultures grown with and without serum to release metabolically labeled tritriated purine compounds in response to depolarization. Exposure to 54 mM potassium stimulated release of adenosine, inosine, and hypoxanthine from both serum-supplemented and defined-medium cultures. However, depolarization-stimulated release of adenine nucleotides was observed only from serum-supplemented cultures and not from serum-free cultures. The release of adenine nucleotides from serum-containing cultures is affected by divalent cations in the manner expected for a neurosecretory process. The failure of serum-free cultures to release detectable adenine nucleotides raises the possibility that they do not share with, or that they differ from, serum-supplemented cultures in the purinergic aspect of the multiple transmission modes available to sympathetic neurons, and that this difference may be due to effects of the culture medium.

Additional Information

© 1985 Society for Neuroscience. For the first six months after publication SfN's license will be exclusive. Beginning six months after publication the Work will be made freely available to the public on SfN's website to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). Received July 2, 1984; Revised October 5, 1984; Accepted October 8, 1984. This work was supported by grants from the National Institute of Neurological Disorders and Stroke. E. J. W. was a predoctoral trainee of the National Institute of General Medical Sciences. P. H. P. was a Rita Allen Foundation Fellow and a McKnight Foundation Neuroscience Development Awardee. Support was also provided by grants from the National Institute of Neurological and Communicative Disorders and Stroke to P. H. P. We are grateful to Drs. K. Yoshioka and T. M. Jessell for sharing their data, methods, and facilities and to Dr. W. D. Matthew for providing laboratory space. We also thank Drs. S. C. Landis and T. M. Jessell for helpful discussions of the manuscript.

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