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Cytosine arabinoside kills postmitotic neurons in a fashion resembling trophic factor deprivation: evidence that a deoxycytidine-dependent process may be required for nerve growth factor signal transduction

DP Martin, TL Wallace and EM Johnson Jr
Journal of Neuroscience 1 January 1990, 10 (1) 184-193; DOI: https://doi.org/10.1523/JNEUROSCI.10-01-00184.1990
DP Martin
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
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TL Wallace
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
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EM Johnson Jr
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
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Abstract

Cytosine arabinoside (AraC) is a pyrimidine antimetabolite that kills proliferating cells by inhibiting DNA synthesis. In this paper we report that AraC kills postmitotic rat sympathetic neurons in a fashion similar to the neuronal death that follows nerve growth factor (NGF) deprivation. Postmitotic rat sympathetic neurons were cultured for 1 week in the presence of NGF and then treated with AraC, still in the presence of NGF. AraC killed neurons after 4 d with an EC50 of 50 microns. The morphological and temporal characteristics of neuronal death that began around 3 d after addition of AraC were indistinguishable from those observed beginning 24 hr after NGF deprivation. Death caused by AraC was prevented by the same agents that prevent the death of NGF-deprived neurons, which included inhibitors of RNA and protein synthesis, a cAMP analog, and depolarizing concentrations of KCl. In contrast, neuronal death caused by ultraviolet irradiation, ricin toxin, and a variety of other toxic insults did not share these morphological, biochemical, or temporal characteristics. Other antimitotic drugs, including adenine arabinoside, thymine arabinoside, fluorodeoxyuridine, hydroxyurea, and aphidicolin, did not kill neurons. AraC caused neurons to behave as if deprived of NGF by interfering with deoxycytidine (dC) metabolism distinct from DNA biosynthesis. dC entirely prevented the neurotoxicity of AraC, even when present at a concentration 1000-fold less than that of AraC. Other deoxynucleosides, and cytidine, did not prevent AraC neurotoxicity. dC could not, however, substitute for NGF and thus is unlikely to be a direct mediator of NGF action. It is hypothesized that dC may participate in a pathway, distinct from DNA synthesis, that is necessary for neurons to respond to exogenous trophic factors.

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The Journal of Neuroscience: 10 (1)
Journal of Neuroscience
Vol. 10, Issue 1
1 Jan 1990
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Cytosine arabinoside kills postmitotic neurons in a fashion resembling trophic factor deprivation: evidence that a deoxycytidine-dependent process may be required for nerve growth factor signal transduction
DP Martin, TL Wallace, EM Johnson Jr
Journal of Neuroscience 1 January 1990, 10 (1) 184-193; DOI: 10.1523/JNEUROSCI.10-01-00184.1990

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Cytosine arabinoside kills postmitotic neurons in a fashion resembling trophic factor deprivation: evidence that a deoxycytidine-dependent process may be required for nerve growth factor signal transduction
DP Martin, TL Wallace, EM Johnson Jr
Journal of Neuroscience 1 January 1990, 10 (1) 184-193; DOI: 10.1523/JNEUROSCI.10-01-00184.1990
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